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Biodefense Reference Library
Foreign Animal and Zoonotic Disease Center
One Medicine: One Health (Zoonotic Disease) Online Course
Presented
by
Stephen M. Apatow,
Director of Research and Development
Humanitarian Resource
Institute Biodefense Reference Library
Foreign Animal and Zoonotic Disease Center
[Vitae][Email]
ZOONOTIC DISEASES
BACTERIAL
BRUCELLOSIS
U.S. Centers for Disease Control and Prevention: Division of Bacterial
and Mycotic Diseases
Brucellosis: General
Information | Technical
Information | Additional
Information
Disease Overview: Institutional Animal Care
and Use Committee, University of California, Santa Barbara.
(In humans: Mediterranean fever, undulant fever, Malta fever. In
animals: contagious abortion, epizootic abortion, Bang's disease)
AGENT:
Brucella abortus: cattle, sheep Brucella canis: dogs Brucella melitensis:
sheep, goats Brucella suis: swine.
RESERVOIR
AND INCIDENCE
Of the above species, Brucella canis is most likely zoonotic agent
in the lab animal facility due to the extensive use of random source and lab
bred dogs, in contrast to use of large domestic animals. Prevalence: 1 to
10% in dogs, throughout the U.S. B. canis is well adapted to dogs, and is
not the subject of a large scale eradication program in the general dog population,
as Brucella has been in other animals. Human brucellosis due to B. canis
is uncommon but can be acquired from dogs; most cases resulted from contact
with aborting bitches. In 1988, the CDC noted 96 cases of brucellosis reported
in the U.S.: 22 from Texas and 20 from Calif.
TRANSMISSION:
Ingestion of unpasteurized milk Lab accidents Poorly defined transmission
cycle in zoonotic diseases: contact with infected animals especially aborted
fetuses, fluids or membranes, or urine. Possibly airborne.
DISEASE
IN ANIMALS:
Abortions are followed by immunity, though carrier state persists
especially with secretions from the udder. infertility, testicular abnormalities,
poor semen quality in dogs. inapparent infection may be common, as indicated
by seropositivity.
DISEASE
IN MAN:
Lymphadenopathy, splenomegaly, fever, headache, chills, orchitis,
weakness, nausea, weight loss. The chronic form may assume an undulant nature,
with periods of normal temperature between acute attacks; symptoms may persist
for years, either continuously or intermittently. Antibiotics can effect a
cure within one year in about 80% of cases. Case fatality if untreated is
less than 2%.
DIAGNOSIS:
Rapid slide agglutination test is available. Blood culture and
additional serologic tests used to confirm slide test results.
TREATMENT:
Single-drug regimens are not recommended because the relapse rate
may be as high as 50%. Combination regimens of two or three drugs are more
effective. Either (1) doxycycline plus rifampin or streptomycin (or both)
(2) trimethoprim-sulfamethoxazole plus rifampin or streptomycin (or both)
are effective in doses for 21 days. Longer courses of therapy may be required
to cure relapses, osteomyelitis, or meningitis.
PREVENTION\CONTROL:
Quarantine and test Disposable gloves Chlorine, organic iodine,
quaternary ammonium compounds are rapid bactericidal agents.
SALMONELLOSIS
U.S. Centers for Disease Control and Prevention: Division of Bacterial
and Mycotic Diseases
Salmonellosis: General
Information | Technical
Information | Additional
Information
Office International des Epizooties
Salmonellosis:
Manual of standards Diagnostic Tests and Vaccines 2000
Disease Overview: Institutional Animal Care
and Use Committee, University of California, Santa Barbara.
(Salmonella food poisoning, enteric paratyphosis) A common bacterial
cause of food-poisoning worldwide. Over 1800 food-poisoning serotypes of salmonella
(bacterium) exist. The prevalence of individual serotypes constantly changes.
In the U.S., 5 million cases are diagnosed annually. S. typhi, the cause
of Typhoid Fever, rarely occurs in the U.S. and is not discussed here.
RESERVOIR
AND MODE OF TRANSMISSION:
Salmonellas are common commensals of all animals and birds and
are excreted in feces. Host-adapted strains may cause serious illness (e.g.,
S. dublin in cattle, S. pullorum in chickens), but most human food-poisoning
salmonellas do not cause clinical signs in animals. The main reservoirs for
human infection are poultry, cattle, sheep and pigs. Infection in animals
is maintained by recycling slaughterhouse waste as animal feed, fecal oral
spread and fecal contamination of hatching eggs. Transmission occurs when
organisms, introduced into the kitchen in poultry carcasses, meat or unpasteurized
milk, multiply in food owing to inadequate cooking, cross-contamination
of cooked foods and inadequate storage. Person-to-person spread is common
in institutions such as hospitals. The organism inhabits the intestinal tract
of many animals including birds, cattle, sheep, pigs, lab. animals (rats,
mice, hamsters, guinea pigs, nonhuman primates) and humans. Salmonella occurs
worldwide. *The house mouse may also be a reservoir of the infection and may
play a role in human and animal salmonellosis. Humans, rarely, and animals
may be carriers and asymptomatic shedders of the organism. *Salmonella prevalence
in the U.S. canine population may be 10% or more. *Prevalence data from 8
studies conducted worldwide indicated that a wide range (0.6-27%) of cats
were culture-positive for Salmonella. *Salmonella carriers in newly imported
Rhesus and Cynomolgus monkeys exceeded 20% in some shipments. *Birds, reptiles,
and turtles are especially dangerous sources of Salmonellosis. 94% of all
reptiles harbor Salmonella. Turtles alone in 1970 may have caused 280,000
human cases of Salmonellosis. *In 1975 the FDA ruled it illegal to sell a.
Viable Turtle eggs b. Live turtles with a carapace length < 10.2cm (4 inches)
c. Exceptions - Educational & scientific institutions and marine turtles.
d. Marine turtles have not been shown to be a reservoir of Salmonella
TRANSMISSION:
Indirect transmission via contaminated food and water are the most
common sources but transmission may also be by direct contact. It is a common
contaminant of sewage. Found in many environmental water sources. Environmental
contamination continues to be a potential source of infection for lab animals
and secondarily for personnel handling those animals. *Animal feed containing
animal by products continues to be a source of Salmonella contamination,
especially if the diets consist of raw meal and have not undergone the pelleting
process.
INCUBATION
PERIOD:
Humans. 12-72 hours. Animals. 1-5 days.
CLINICAL
FEATURES:
Humans.The presence and severity of symptoms depends on the infecting
dose. Typically there is watery diarrhoea for about ten days, possibly leading
to dehydration, with abdominal pain and low-grade fever. Septicemia and abscess
formation are rare. Animals. Subclinical infection is common and many animals
may be intermittent or persistent carriers. However, cows may suffer with
fever, diarrhoea and abortion. Calves undergo epizootic outbreaks of diarrhoea
with high mortality. In pigs, fever and diarrhoea are less common than in
cattle. Infected sheep, goats and poultry usually show no signs of infection.
PATHOLOGY:
Humans. Enteritis is a feature. Extraintestinal infection may cause
abscesses. Animals. Penetration of the infection into the mucosa is followed
by inflammation, especially ileitis, progressing to inflamed mesenteric lymph
nodes in the mesentery, possibly progressing to septicemia and pneumonia especially
in calves. Dehydration and rapid loss of weight are due to stimulation of
chloride excretion and inhibition of sodium absorption. Abortion in cattle
is caused by massive proliferation of salmonella in the placenta leading to
placental necrosis.
DIAGNOSIS:
Humans. Isolate salmonella from feces and suspected foods using
selective media followed by serotyping and, if appropriate, phage typing.
Animals. Culture feces, postmortem tissues and foods of animal origin. Serological
tests are of limited value as many noninfected animals have titers from past
infections. Humans. Usually only a self-limiting illness occurs. Deaths
from dehydration or septicemia are rare and occur usually in infants, or
debilitated or elderly patients. Animals.There is abortion in cattle and
endometritis with temporary infertility. In calves, dehydration and septicemia
may lead to death.
PREVENTION:
Humans. Educate food handlers in good kitchen hygiene. Ensure thorough
cooking of meat, refrigerate cooked foods and prevent cross-contamination.
Pasteurize all milk. Ensure personal hygiene. Reduce contamination of poultry
carcasses at abattoirs. Irradiation of meat and other foods before purchase
will reduce contamination. Animals. This is difficult and often impractical
because there are many sources of infection. Principles of control include
the following: maintain closed herds and flocks; keep animals in small groups;
purchase replacements direct from the farm of origin; avoid mixing animals
from different sources; sterilize ingredients of animal feed; provide mains
drinking water for grazing livestock; prevent access of wild birds and rodents
to animal houses; completely destock animals and thoroughly cleanse and disinfect
housing between batches; monitor poultry breeding stock and remove excreters;
disinfect hatching eggs and fumigate incubators.
TREATMENT:
Humans. Treatment of uncomplicated enterocolitis is symptomatic
only. Young, malnourished, or immunocompromised infants, severely ill patients,
those with sickle cell disease, and those with suspected bacteremia should
be treated for 3-5 days with trimethoprim-sulfamethoxazole (one double-strength
tablet twice a day), ampicillin (100 mg/kg IV or orally), or ciprofloxacin
9750 mg twice daily). Animals. Treatment with antibiotics and sulfonamides
immediately diarrhoea and fever occur reduces mortality but is contraindicated
in healthy carriers in which treatment may prolong the carrier state.
VACCINATION:
Humans. None. Animals. Vaccines are available against S. dublin
and S. typhimurium in calves. A live vaccine prepared from a rough strain
of S. dublin gives good protection in calves against both S. dublin and S.
typhimurium.
LEGISLATION:
Humans. The disease is notifiable specifically in the USA, Australia,
New Zealand and several European countries, or as food-poisoning as in the
UK. Animals. Notification of infection in food animals is obligatory in some
countries, including the UK, with statutory sampling of animal protein for
animal feed. Heat treatment of waste food applies in the UK. A slaughter
policy is claimed in Luxembourg, Germany and Czechoslovakia.
SHIGELLOSIS
U.S. Centers for Disease Control and Prevention: Division of Bacterial
and Mycotic Diseases
Shigellosis: General
Information | Technical
Information | Additional
Information
Disease Overview: Institutional Animal Care
and Use Committee, University of California, Santa Barbara.
SYNONYM:
Bacillary dysentery.
ETIOLOGY:
The type species is Shigella dysenteriae, other agents are S. flexneri,
S. boydii, and S. sonnei. The first three species are subdivided into serotypes.
GEOGRAPHIC
DISTRIBUTION:
Worldwide.
THE DISEASE
IN MAN:
It is seen most often in preschool-age children. A new serotype
introduced into tropical areas where the population is undernourished provokes
disease in all age groups, particularly children, the elderly, and debilitated
individuals. Generally, the incubation period is less than 4 days. The disease
begins with fever and abdominal pains, followed by diarrhea and dehydration
for 1 to 3 days. A second phase of the symptomatology can last for several
weeks. The main symptom is tenesmus; in serious cases, stools contain blood,
mucus, and pus. The symptomatology is usually variable. In many countries,
strains of Shigella resistant to sulfonamides and to several antibiotics have
been observed.
THE DISEASE
IN ANIMALS:
A clinical picture similar to that in man occurs in monkeys.
SOURCE
OF INFECTION AND MODE OF TRANSMISSION:
The principal reservoir of the infection for man is other humans
that are sick or carriers. The sources of the infection are feces and contaminated
objects. The most common mode of transmission is the fecal-oral route. Outbreaks
comprising numerous cases have had their origin in a common source of infection,
such as foods contaminated by hands or feces of carrier individuals. Insects,
particularly flies, can also play a role as mechanical vectors. Bacillary
dysentery is a serious disease with high mortality in nonhuman primates
in captivity, but there is doubt that monkeys can harbor the etiologic agent
in their natural habitat. Monkeys probably contract the infection by contact
with infected humans. The infection spreads rapidly in nonhuman primate colonies
because the monkeys defecate on the cage floor and also often throw their
food there.
ROLE OF
ANIMALS IN THE EPIDEMIOLOGY OF THE DISEASE:
Of little significance. Cases of human bacillary dysentery contracted
from nonhuman primates are known. The victims are mainly children. In highly
endemic areas, dogs may shed Shigella temporarily. The etiologic agent has
also been isolated from horses, bats, and rattlesnakes. Nevertheless, animals
other than nonhuman primates play an insignificant role.
DIAGNOSIS:
Definitive diagnosis depends on isolation of the etiologic agent
by culture of fecal material on selective media. Serologic identification
and typing are important from the epidemiologic viewpoint.
TREATMENT:
In humans, treatment of dehydration and hypotension is lifesaving
in severe cases. The current antimicrobial treatment of choice is trimethoprim-sulfamethoxazole
(one double-strength tablet twice a day), or ciprofloxacin (750 mg twice
a day; contraindicated in children and pregnant women). Parental hydration
and correction of acidosis and electrolyte disturbances are of primary importance.Antispasmodics
(e.g., tincture of belladonna) are helpful when cramps are severe. Drugs that
inhibit intestinal peristalsis (paregoric, diphenoxylate with atropine) may
ameliorate symptoms but prolong fever, diarrhea, and excretion of Shigella
in feces. Appropriate precautions should be taken both in the hospital and
in the home to limit spread of infection.
CONTROL:
In man, control methods include a) environmental hygiene, especially
disposal of human waste and provision for potable water; b) personal hygiene;
c) education of the public and of food handlers about the sources of infection
and methods of transmission; d) sanitary supervision of the production, preparation,
and preservation of foods: e) control of flies; f) reporting and isolation
of cases and sanitary disposal of feces; and g) search for contacts and
the source of infection. A live, streptomycin-dependent vaccine, administered
orally in three or four doses has given good protection against the clinical
disease for 6 to 12 months. Its use is indicated in institutions where shigellosis
is endemic. Indiscriminate use of antibiotics must be avoided tn order to
prevent the emergence of multiresistant strains and to ensure that these medications
remain available for use in severe cases. In animals, control consists of
a) isolation and treatment of sick or carrier monkeys: b) careful cleaning
and sterilization of cages; c) prevention of crowding in cages: and d) prompt
disposal of wastes and control of insects.
YERSINIA
U.S. Centers for Disease Control and Prevention: Division of Bacterial
and Mycotic Diseases
Yersinia enterocolitica: General
Information | Technical Information | Additional Information
Disease Overview: Institutional Animal Care
and Use Committee, University of California, Santa Barbara.
Laboratory animals are susceptible to three Yersinia species that
are potentially zoonotic:
AGENT:
Gram negative, non spore forming rods.
1. YERSINIA PSEUDOTUBERCULOSIS AND ENTEROCOLITICA
(Pseudotuberculosis)
RESERVOIR
AND INCIDENCE
Ubiquitous in nature, isolated from dust, soil, water, milk. Natural
infections occur in man, birds, rodents, rabbits , guinea pigs, mice, cats,
nonhuman primates, sheep, swine, goats.
TRANSMISSION:
Direct contact, or fecal contaminated food or water cause most
transmission from animals to man. Human cases of have been reported in association
with disease in household pets, particularly sick puppies and kittens. The
most important source of Y. enterocolitica infection may be pork, as the pharynx
of pigs may be heavily colonized.
DISEASE
IN ANIMALS:
Guinea pigs, rabbits, and hamsters exhibit poor condition and enlarged
lymph nodes. Subacute clinical signs are common, with diarrhea and weight
loss, possibly death within 2 weeks to 3 months. Chinchillas are very susceptible
to infection with Y. enterocolitica. In sheep, abortions, epididymitis and
orchitis occur with high mortality. In cattle, abortion and pneumonia occur.
Nonhuman primates exhibit an ulcerative colitis. Histopathological lesions
include acute inflammation of the terminal ileum with mesenteric lymphadenitis
occurs. Sometimes abscesses develop in the liver, spleen, and lungs. Usually
self-limiting, but there is a fatality rate of 5-7%.
DISEASE
IN MAN:
Acute watery diarrhea, mesenteric lymphadenitis which can be confused
with appendicitis, fever, headache, pharyngitis, anorexia, vomiting erythema
nodosum (in about 10% of adults), post-infectious arthritis, iritis, cutaneous
ulceration, hepatosplenic abscesses, osteomyelitis and septicemia.
DIAGNOSIS:
Fecal culture using cold enrichment technique. Serologic diagnosis
can be made by an agglutination test or by ELISA.
TREATMENT:
Usually resistant to penicillin and its derivatives. Agents of
choice are the aminoglycosides and cotrimoxazole. Both are usually sensitive
to the tetracyclines.
PREVENTION/CONTROL:
Control rodents and prevent contamination of food and water by
rodents and birds. Pasteurize milk. Cook pork thoroughly. Personal hygiene
is important.
2. YERSINIA PESTIS
(Plague, Pest, black death, pestilential fever) The second pandemic
of plague, known then as the "Black Death," originated in Mesopotamia about
the middle of the 11th century, attained its height in the 14th century and
did not disappear until the close of the 17th century. It is thought that
the Crusaders, returning from the Holy Land in the 12th and 13th centuries,
were instrumental in hastening the spread of the disease. Again the land along
trade routes was primarily involved and from them the infections spread east,
west, and north. During the course of the disease, 25,000,000 people perished,
a fourth of the population of the world.
AGENT:
A gram negative coccobacillus.
RESERVOIR
AND INCIDENCE
Endemic in wild rodents in Southwestern U.S., as well as in Africa
and Asia. Most important reservoirs worldwide are the domestic rat, Rattus
rattus, and the urban rat, Rattus norvegicus. Human infections have increased
since 1965 and usually result from contact with infected fleas or rodents.
The disease is also associated with cats, goats, camels, rabbits, dogs and
coyotes. Dogs and cats may serve as passive transporters of infected rodent
fleas into the home or laboratory.
TRANSMISSION:
Contact with infected rodent fleas or rodents. Fleas may remain
infected for months. Note: a protein secreted by the Yersinia is a coagulase
that causes blood ingested by the flea to clot in the proventriculus. The
bacillus proliferates in the proventriculus, and thousands of organisms are
regurgitated by obstructed fleas and inoculated intradermally into the skin.
This coagulase is inactive at high temperatures and is thought to explain
the cessation of plague transmission during very hot weather. Pulmonary form
spread by airborne or droplet infection. Human infections from non-rodent
species usually result from direct contact with infected tissues, by scratch
or bite injuries, and handling of infected animals. Several recent reports
have detailed human plague associated with exposure to domestic cats. Exposure
can be from inhalation of respiratory secretions of cats with pneumonic plague
or by contaminating mucous membranes or skin wounds with secretins or exudates.
DISEASE
IN ANIMALS:
dogs usually have a brief self-limiting illness cats usually exhibit
severe and often fatal infection, with fever, lymphadenopathy, hemorrhagic
pneumonia, and encephalitis. rodents may carry the disease asymptomatically
or develop fatal disease. infected rats and squirrels frequently die unless
they are from an enzootic area and have acquired immunity.
DISEASE
IN MAN:
Incubation period 2 to 6 days. In humans the disease is called
Bubonic, Septicemic, or Pneumonic plague depending on the pattern of distribution
of the infection. Bubonic is the most common form causing fever and swollen,
tender lymph nodes (called Buboes). Pneumonic plague is systemic plague with
lung involvement. Mortality may exceed 50%. Plague is also called the "black
death" because disseminated intravascular coagulation takes place and areas
of skin undergo necrosis.
DIAGNOSIS:
Impression smears of aspirates or blood stained with gram or Giemsa.
Organisms have a typical "safety pin" appearance culture of the organisms
can be performed, by reference lab FA of smear is confirmatory. Serology via
Complement fixation, passive hemagglutination, and immunofluorescence (IFA)
TREATMENT:
Streptomycin with tetracycline or chloramphenicol.
PREVENTION\CONTROL:
Wild rodents should be controlled and fleas should be eliminated.
It is important to control rodents and fleas for outdoor housed animals. Sentinel
animal programs used in endemic areas. Endemic areas of the U.S. include
California, Nevada, Arizona, and New Mexico. Masks gowns, and gloves should
be worn when handling cats suspected to be infected and all contaminated surfaces
disinfected. Notify Health Department of suspected cases Vaccines available
for high risk personnel.
TUBERCULOSIS
(Consumption)
AGENT,
RESERVOIR AND INCIDENCE
TB is caused by the gram positive, acid fast, aerobic, bacillus
of the Mycobacterium genera. The most common species of mycobacteria are:
1. M. bovis (cattle, dogs, swine) 2. M. avium (birds, swine, sheep) 3. M.
tuberculosis (man, nonhuman primates, cattle, dogs, swine, psitticines). 4.
M. marinum, fortuitum, platypolcitis (fish) Note: Atypical mycobacterium,
M. scrofulaceum, M. kansasii, and M. intracellulare have been reported in
NHP's and are also present in soil and water. They can cause pulmonary disease
refractory to treatment in man, and are most often seen in immunocompromised
people. Specific reagents can be used to skin test for these bacteria. TB
continues to be a major cause of morbidity and mortality throughout the
world. One billion people are infected with the tubercle bacillus, and there
are 8 million new cases and 3 million deaths annually. Cases of active tuberculosis
are increasing in the United States after years of decline. A provisional
total of 23,720 cases was reported by the end of 1990. Case rates increased
4.4 percent between 1988 and 1989, and perhaps another 1 percent in 1990.
Overall rate was 9.5 per 100,000 in 1989, with the Middle Atlantic and Pacific
regions reporting the highest rates, 36 percent and 34 percent, respectively,
above the U.S. total. The lowest rates were in the West, North, Central, and
Mountain regions. Rates continue to be higher among urbanites, minorities,
the poor, the homeless, substance abusers and persons infected with HIV. All
three types are capable of causing disease in man although M. tuberculosis
(variety hominis) is by far the most common. Nonhuman primates can carry all
three types but most infections are caused by M. tuberculosis variety hominis.
While most nonhuman primates are capable of contracting TB, Old World species
appear to be more susceptible to the disease than New World species and great
apes. Most cases of TB in monkeys are thought to arise from human contact.
Animals may be imported from areas of the world where the incidence of the
disease is high and where contact between humans and simians is frequent.
In close confinement the disease can spread rapidly.
TRANSMISSION:
Mycobacterium bacilli are transmitted from infected animals or
infected tissue primarily via the aerosol route. May also be contracted via
ingestion or cutaneous inoculation of the bacilli. Personnel caring for infected
animals as well as those performing necropsies on infected animals are at
risk for contracting the disease. Exposure to dusty bedding of infected animals,
coughing of infected animals, and aerosolization of the organism during sanitation
procedures may also be sources of the disease in the lab environment. Once
within the body the organism may spread throughout the lungs, lymphatics,
blood vascular system, and many visceral organs.
DISEASE
IN NONHUMAN PRIMATES:
The signs of TB may be insidious with only slight behavioral changes
noticed, followed by anorexia and lethargy. Often animals die suddenly while
appearing to be in good condition. Other signs which might be seen include
diarrhea, suppuration of lymph nodes, ulceration of the skin, and palpable
splenomegaly and hepatomegaly. The organ of predilection is the lung but
lesions may also be seen in the pleura, intestines, lymph nodes, liver, kidney,
spleen, and peritoneum. Under the surface of these tissues are yellowish-white
to gray nodules filled with caseous material which may rupture and produce
cavitation. Although skeletal involvement in primates is rare, tuberculosis
of the spine may cause paralysis of the hindlimbs (Pott's disease).
DISEASE
IN FISH:
In infected fish, granulomatous lesions are usually observed.
DISEASE
IN MAN:
In humans the clinical signs depend on the organ system involved.
The most familiar signs related to pulmonary TB are cough, sputum production,
and hemoptysis. The patient may be asymptomatic for years. General signs may
include anorexia, weight loss, lassitude, fatigue, fever, chills and cachexia.
Skin lesions are characterized by ulcers or by papular lesions progressing
to dark suppurative lesions. TB may affect virtually every other organ system
with signs or symptoms relating to the individual system. Miliary TB is most
often seen in the very young and old people.
DIAGNOSIS:
The diagnosis of TB is often difficult. Four tests are commonly
used for presumptive diagnosis: 1. Intradermal TB test - Mammalian tuberculin
2. Radiography 3. Acid fast stained sputum smear 4. ELISA Confirmation by
culture, histopath, or animal inoculation.
TREATMENT:
Regimens currently accepted in the USA include isoniazid combined
with rifampin, with or without pyrazinamide.
PREVENTION\CONTROL:
Multifaceted and includes: personnel education wearing of protective
clothing when handling nonhuman primates a regular health surveillance program
for humans and nonhuman primates isolation and quarantine of suspect animals
rapid euthanasia and careful disposal of infected animals Vaccine - A vaccine,
BCG, is available (Bacille Calmette-Guerin, strain of M. Bovis) a. Used in
humans quite often in G. Britain b. Used in high risk groups c. Effective,
but it causes the patient to have a positive TB test. Personnel working with
NHP's who convert to a positive skin test should be referred for appropriate
medical treatment and follow up and should not work with animals until shown
to be noninfectious.
LEPROSY
U.S. Centers for Disease Control and Prevention: Division of Bacterial
and Mycotic Diseases
Leprosy: See: Hansen's
Disease
Disease Overview: Institutional Animal Care
and Use Committee, University of California, Santa Barbara.
SYNONYM:
Hansen's disease.
ETIOLOGY:
Mycobacterium leprae, a polymorphic acid-alcohol-fast bacillus.
M. leprae is hard to distinguish from other unculturable mycobacteria naturally
infecting animals. The failure of attempts to culture M. leprae in vitro constitutes
a great barrier to better determining its biochemical characteristics for
identification purposes as well as for therapeutic and immunologic studies.
In part, this difficulty has been overcome, first, by in vivo culture on mouse
foot pads and, lately, by the discovery that the leprosy organism can infect
the nine-banded armadillo (Dasypus novemcinctus). At present, the latter
serves as a model for lepromatous leprosy and provides a large number of
bacilli for research.
OCCURRENCE
IN MAN:
An estimated 12 million people are affected by leprosy. The highest
prevalence is in tropical and subtropical regions of Asia, Africa, Latin America,
and Oceania. Leprosy is very prevalent in India, Southeast Asia, the Philippines,
Korea, southern China, Papua New Guinea, and some pacific islands. Ninety
percent of the cases reported in the Americas come from five countries: Argentina,
Brazil, Colombia, Mexico, and Venezuela. Chile is the only South American
country free of the infection. In the United States 2,500 cases are known,
most of them in immigrants. Autochthonous cases arise in Hawaii, Puerto Rico,
Texas, and Louisiana. The infection's prevalence is related to the socioeconomic
level of the population. The fact that the disease has practically disappeared
in Europe is attributed to the improved standard of living there. The proportion
of total leprosy cases represented by lepromatous leprosy (see The Disease
in Man) varies with the region. In Asia and the Americas this form makes
up between 25 and 65% of all cases, while in Africa it accounts for only
6 to 20%.
THE DISEASE
IN MAN:
The incubation period is usually 3 to 5 years, but it can vary
from 6 months to 10 years or more. Clinical forms of leprosy cover a wide
spectrum, ranging from mild self-healing lesions to a progressive and destructive
chronic disease. The polar form at one end of the spectrum is tuberculoid
leprosy, and at the other, lepromatous leprosy. Intermediate forms are also
found. Tuberculoid leprosy is characterized by localized lesions of the skin
and nerves, often asymptomatic. Basically, the lesions consist of a granulomatous,
paucibacillary, inflammatory process. The bacilli are difficult to detect,
and can be observed most frequently in the nerve endings of the skin. This
form results from active destruction of the bacilli by the cellular immunity
of the patient. On the other hand, serum antibody titers are generally low.
Nerve destruction causes lowered conduction; heat sensibility is the most
affected, tactile sensibility less so. Trophic and autonomic changes are common,
especially ulcers on the sole and mutilation of body members. Lepromatous
leprosy is characterized by numerous symmetrical skin lesions consisting of
macules and diffuse infiltrations, plaques, and nodules of varying sizes
(lepromas). There is involvement of the mucosa of the upper respiratory
tract, of lymph nodes, liver, spleen, and testicles. Infiltrates are basically
histiocytes with a few lymphocytes. Cellular immunity is absent (negative
reaction to lepromin) and antibody titers are high. In this form of the disease,
as in the borderline, erythema nodosum leprosum (ENL) often appears. The
indeterminate form of leprosy has still not been adequately characterized
from the clinical point of view; it is considered to be the initial stage
of the disease. The first cutaneous lesions are flat, hypopigmented, and
have ill-defined borders. If this form is not treated, it may develop into
tuberculoid, borderline, or lepromatous leprosy. Bacilli are few, and it
is difficult to confirm their presence. Finally, the borderline form occupies
a position intermediate between the two polar forms (tuberculoid and lepromatous),
and shares properties of both; it is unstable and may progress in either
direction. Destruction of nerve trunks may be extensive. Bacilli are observed
in scrapings taken from skin lesions. An estimated one-third of clinical
cases become incapacitated. half of them completely. Nevertheless, these
proportions are now changing, due to both prevention/control programs and
early implementation of effective treatments. There is evidence that inapparent
infection may occur with a certain frequency among persons, especially family
members, in contact with patients.
THE DISEASE
IN ANIMALS:
The disease in armadillos (Dasypus novemcinctus) is similar to
the lepromatous form in man. Infection in these animals is characterized by
macrophage infiltrates containing a large number of bacilli. Skin lesions
vary from mild to severe. The small dermal nerves are invaded by the etiologic
agent. Many bacilli are seen in the macrophages of the lymph tissue, in the
pulp of the spleen, and in Kupffer's cells in the liver. M. leprae is known
to prefer the coolish parts of the human or mouse body. For this reason, armadillos
were used as experimental animals even before natural inaction was confirmed
in them, since their body temperature is from 30 to 35oC. Experimental inoculation
of armadillos with human leproma material reproduces the disease, characterized
by broad dissemination of the agent, and involvement of lymph glands, liver,
spleen, lungs, bone marrow, meninges, and other issues, in a more intense
form than is usually observed in man. The disease in the chimpanzee appeared
as a progressive chronic dermatitis with nodular thickening of the skin of
the ears, eyebrow nose, and lips. Lesions of the nose, skin, and dermal nerves
contained copious quantities of acid-fast bacteria. The case was histologically
classified as borderline 12 months after the clinical symptoms were first
observed, and as lepromatous after a later biopsy. In the case of the Cercocebus
monkey, the initial lesion consisted of nodules on the face. Four months later,
a massive infiltration and ulceration were seen on the face and nodules appeared
on the car and the forearms. Sixteen months after cutaneous lesions were
first observed. The animal began to suffer deformities and paralysis of the
extremities. Histopathologic findings indicated the subpolar or intermediate
lepromatous form. The disease was progressive, with neuropathic deformation
of feet and hands. It seemed to regress when specific treatment was administered.
The animal apparently contracted the disease from a patient with active leprosy.
Experimental infections carried out to date have indicated that these animals
may experience a spectrum of different forms similar to those in man.
SOURCE
OF INFECTION AND MODE OF TRANSMISSION:
Man is the principal reservoir of M. leprae. The method of transmission
is still not well known due to the extended incubation period. Nevertheless,
the principal source of infection is believed to be lepromatous patients,
in whom the infection is multibacillary, skin lesions are often ulcerous,
and a great number of bacilli are shed through the nose similarly. Bacilli
are found in the mouth and pharynx. Consequently, transmission might be
effected by contact with infected skin, especially through wounds or abrasions,
and by aerosols, as is the case in tuberculosis. Lately, more importance
has been attributed to aerosol transmission. Oral transmission and transmission
by hematophagous arthropods are not discounted, but they are assigned less
epidemiologic importance. Until recently, leprosy was believed to be an
exclusively human disease. But research in recent years has demonstrated
that the infection and the disease also occur naturally in wild animals.
Even though some researchers have expressed doubt that the animal infection
is identical to the human, at present an accumulation of evidence indicates
that the etiologic agent is the same. The origin of infection in animals
is unknown. It is believed that armadillos contracted the infection from
a human source, perhaps from multibacillary patients before the era of sulfones.
In this regard, it should be pointed out that leprosy bacilli may remain
viable for a week in dried nasal secretions and that armadillos are in close
contact with the soil. The high disease prevalence in some localities would
indicate armadillos can transmit the infection to one another, either by
inhalation or direct contact. Another possible transmission vehicle is maternal
milk, in which the agent has been detected. It is difficult to demonstrate
that armadillos are a source infection for man because of the long incubation
period in humans and the impossibility of excluding a human source in an
endemic area. In Texas, a case of human leprosy was attributed to a patient's
practice of capturing armadillos and eating their meat. Subsequently, another
five cases with hand lesions were detected in natives of the same state who
habitually hunted and cleaned armadillos but had no known contact with human
cases. The prevalence of leprosy in armadillos in Louisiana and Texas suggests
that these animals could serve as a reservoir of M. leprae; however, nothing
is known about the frequency of infection in nonhuman primates and the role
they may play in transmission of the disease. The sources of the cases of
leprosy in these animals were probably people with lepromatous leprosy.
DIAGNOSIS:
Laboratory confirmation of leprosy requires the demonstration of
acid-fast bacilli in scrapings from slit skin smears or the nasal septum.
Biopsy of skin or of a thickened involved nerve also gives a typical histologic
picture. M. leprae does not grow in artificial media.
CONTROL:
Control is based on early detection and chemotherapy. In the face
of multiple confirmed cases of resistance to dapsone, combination of this
medication with rifampicin is presently recommended for paucibacillary leprosy,
and the same two medications in combination with clofazimine for multibacillary
leprosy. Rifampicin has a rapid bactericidal effect and eliminates contagion
in patients in 1 to 2 weeks. The isolation of patients in leprosariums is
no longer necessary, since the chemotherapy effectively eliminates infectiousness
and thereby interrupts transmission of the disease.
VIBRIOSIS
U.S. Centers for Disease Control and Prevention: Division of Bacterial
and Mycotic Diseases
Vibrio parahaemolyticus: General
Information | Technical
Information | Additional
Information
Vibrio vulnificus: General
Information | Technical
Information | Additional
Information
Disease Overview: Institutional Animal Care
and Use Committee, University of California, Santa Barbara.
Vibrios other than Vibrio cholerae that cause human disease are
Vibrio parahaemolyticus, Vibrio vulnificus and Vibrio alginolyticus. All are
halophilic marine organisms. Infection is acquired by exposure to organisms
in contaminated, undercooked, or raw crustaceans or shellfish and warm ( 20o
C) ocean waters and estuaries. Infections are more common during the summer
months from regions along the Atlantic coast and the Gulf of Mexico in the
United States and from tropical waters around the world. Oysters are implicated
in up to 90% of food-related cases. V. parahaemolyticus causes an acute watery
diarrhea with crampy abdominal pain and fever, typically occurring within
24 hours after ingestion of contaminated shellfish. The disease is self-limited,
and antimicrobial therapy is usually not necessary. V. parahaemolyticus may
also cause cellulitis and sepsis, though these findings are more characteristic
of V. vulnificus infection. V. vulnificus and V. alginolyticus-neither of
which is associated with diarrheal illness-are important causes of cellulitis
and primary bacteremia, which may follow ingestion of contaminated shellfish
or exposure to sea water. Cellulitis with or without sepsis may be accompanied
by bulla formation and necrosis with extensive soft tissue destruction, at
times requiring debridement and amputation. The infection can be rapidly
progressive and is particularly severe in immunocompromised individuals-especially
those with cirrhosis-with death rates as high as 50%. Patients with chronic
liver disease and those who are immunocompromised should be cautioned to
avoid eating raw oysters. Tetracycline at a dose of 500 mg four times a day
is the drug of choice for treatment of suspected or documented primary bacteremia
or cellulitis caused by Vibrio species. V. vulnificus is susceptible in vitro
to penicillin, ampicillin, cephalosporins, chloramphenicol, aminoglycosides,
and fluoroquinolones, and these agents may also be effective. V. parahaemolyticus
and V. alginolyticus produce betalactamase and therefore are resistant to
penicillin and ampicillin, but susceptibilities otherwise are similar to
those listed for V. vulnificus.
LISTERIOSIS
U.S. Centers for Disease Control and Prevention: Division of Bacterial
and Mycotic Diseases
Listeriosis: General
Information | Technical
Information | Additional
Information
Disease Overview: Institutional Animal Care
and Use Committee, University of California, Santa Barbara.
(Circling disease)
AGENT
Listeria monocytogenes, gram positive, pleomorphic rod
RESERVOIR
AND INCIDENCE
Isolated from fish, birds, swine, horses, ruminants, guinea pigs,
ferrets, gerbils, rabbits, and chinchillas. The principle reservoir of the
organism is in forage, water, mud, and silage. The seasonal use of silage
as fodder is frequently followed by an increased incidence of listeriosis
in animals.
TRANSMISSION:
Outbreaks have been reported associated with ingestion of unpasteurized
milk and cheese and contaminated vegetables; some sporadic cases may also
be due to foodborne transmission. Refrigeration of foods may provide selective
growth of Listeria. Papular lesions on hands and arms may occur from direct
contact with infectious material or soil contaminated with infected animal
feces. In neonatal infections, the organism may have been transmitted from
mother to fetus in utero or during passage through the infected birth canal.
Person-to-person transmission through venereal contact is possible, as is
infection from inhalation of the organism.
DISEASE
IN ANIMALS:
Two forms exist, the meningoencephalitic and visceral. The former
involves neurological signs with dullness and somnolence. Drooling and lack
of interest in food and mastication soon follow. There is lateral deviation
of the head with a tendency to circle. Paralysis then sets in with recumbency
and death from respiratory failure. The visceral from involves abortion, with
retained placenta. Microabscesses occur throughout the brain. Visceral lesions
involve multiple foci of necrosis in the liver, spleen and heart. Placental
lesions are characteristic with yellow necrotic foci and multiple granulomas
in the fetal liver. Abscess formation in the eye can lead to blindness. Fatality
is very high, approaching 3-30% in outbreaks.
DISEASE
IN MAN:
Symptomless fecal carriage is common. Fever, headache, nausea,
vomiting, endocarditis, granulomatous lesions in multiple organs, cutaneous
involvement, coryza, conjunctivitis, metritis with abortion, sepsis, &
meningitis. Granulomatous lesions and abscesses occur in the liver and other
organs and beneath the skin. Focal necrosis in the placenta with mononuclear
infiltration is seen. Fatality rates may exceed 20%.
DIAGNOSIS:
culture and isolation (special media required). Serologic tests
are unreliable because of cross reactions with other bacterial species.
TREATMENT:
Ampicillin plus an aminoglycoside or Trimethoprim-sulfamethoxazole.
PREVENTION\CONTROL:
Caution and protective clothing when handling infected tissues.
Pregnant women and immunocompromised individuals should avoid contact with
potentially infective materials such as aborted animal fetuses and known infected
persons; they should eat only properly cooked meats and pasteurized dairy
products.
LEPTOSPIROSIS
U.S. Centers for Disease Control and Prevention: Division of Bacterial
and Mycotic Diseases
Leptospirosis: General
Information | Technical
Information | Additional
Information
Office International des Epizooties
Leptospirosis:
Manual of standards Diagnostic Tests and Vaccines 2000
Disease Overview: Institutional Animal Care
and Use Committee, University of California, Santa Barbara.
[Weil's disease, Hemorrhagic jaundice (Leptospira icterohaemorrhagiae),
canicola fever (L. canicola), dairy worker fever (L. hardjo)]
AGENT
Spirochete, Leptospira. Pathogenic leptospires belong to the species
Leptospira interrogans, which is subdivided into more than 200 serovars. The
main natural reservoirs for human infection vary with serovar: L. canicola
in dogs, L. hardjo in cattle, L. pomona in swine, and L. icterohaemorrhagiae
in rats.
RESERVOIR
AND INCIDENCE
Rats, mice, field moles, guinea pigs, gerbils, squirrels, rabbits,
hamsters, reptiles, nonhuman primates, livestock, and dogs. In one study,
40 % of stray dogs were seropositive. Rats and mice are common animal hosts
for L. ballum. Infection in mice is inapparent and can persist for the animal's
lifetime. *Rodents are the only major animal species that can shed leptospires
throughout their life-span without clinical manifestations. Active shedding
by lab animals can go unrecognized until personnel handling the animals
become clinically ill.
TRANSMISSION:
Handling affected animals, contaminating hands, or abrasions with
urine, or aerosol exposure during cage cleaning are most common. The organism
is often transmitted to humans by the urine of the reservoir host. The organism
may also enter through minor skin lesions and probably via the conjunctiva.
Many infections have followed bathing or swimming in infected waters.
DISEASE
IN ANIMALS:
In cattle, fever and anorexia occur with rapid decline in milk
yield and atypical mastitis. Pregnant cows abort with retention of the placenta.
Also, mild jaundice and severe anemia occurs with enlarged and friable liver
and swollen kidneys. In pigs subclinical infection is common, though it can
cause abortion and birth of weak piglets. In dogs and cats, gastroenteritis,
jaundice, and nephritis may occur.
DISEASE
IN MAN:
Ranges from inapparent infection to severe infection and death.
Biphasic Illness a. Weakness, headache, myalgia, malaise, chills, & fever.
b. Leukocytosis, painful orchitis (testes not usually enlarged), conjunctival
effusion, and rash. Icteric leptospirosis (Weil's syndrome-usually caused
by L. icterohaemorrhagiae) is the most severe form of the disease, characterized
by impaired renal and hepatic function, abnormal mental status, hypotension,
and a 5-10% mortality rate. Signs and symptoms are continuous and not biphasic.
DIAGNOSIS:
Early in the disease, the organism may be identified by darkfield
examination of the patient's blood or by culture on a semisolid medium. Culture
is difficult and requires several weeks. A rapid diagnosis is made with the
DOT-ELISA test. *Leptospires can be recovered only from mature mice even
though antibodies can be detected from infected mice of all ages.
TREATMENT:
Penicillins or tetracyclines. Can eliminate L. ballum from a colony
(mice) with 1000 gm chlortetracycline HCL/Ton of feed for ten days.
PREVENTION\CONTROL:
Vaccination in cattle, swine, and dogs Avoid swimming in or drinking
from potentially contaminated water. Protect workers by providing boots and
gloves. Rodent control. Drain wet ground. Doxycycline chemoprophylaxis for
persons at high exposure.
BORRELIOSIS
Disease Overview: Institutional Animal Care
and Use Committee, University of California, Santa Barbara.
(Relapsing fever, tick-borne relapsing fever, spirochetal fever,
vagabond fever, famine fever) A widely distributed bacterial infection spread
from wild rodents by ticks or lice, with high fatality Tick-borne relapsing
fever occurs in Africa, the Americas, Asia and possibly parts of Europe. The
causative agents are Borrelia recurrentis and several other borrelia strains
(bacterium). There is no vaccine.
RESERVOIR
AND MODE OF TRANSMISSION:
Epidemic louse-borne infection is not considered zoonotic. Endemic
tick-borne relapsing fever is transmitted from the natural wild rodent reservoir
by tick bites to humans and dogs. Transovarial transmission in ticks occurs.
Blood-borne person-to-person and intrauterine transmission have been reported.
INCUBATION
PERIOD:
Humans: 1-15 days. Animals.Unknown.
CLINICAL
FEATURES:
Humans. Sudden onset of fever lasting for 3-5 days ends with a
crisis. Then a febrile period of 2-4 days is followed by one to ten or more
recurrences of fever accompanied by severe headaches, nausea, vomiting, diarrhoea,
jaundice and sometimes a macular rash with bleeding due to thrombocytopenia.
Meningitis and cranial nerve involvement are possible. Animals. Arthritis
and fever predominate in infected dogs. The arthritis recurs and may progress
to chronic deformity.
PATHOLOGY:
Humans. Many lesions occur, including enlarged, soft, infarcted
spleen, hepatomegaly, hemorrhages in bone marrow and skin, myocarditis, bronchopneumonia,
and meningitis. Animals. Arthritis, especially of the phalangeal joints,
occurs with the possibility of progression to fibrosis of the joint capsule
and ankylosis.
DIAGNOSIS:
Humans. Identify borrelia in thick blood smears. Otherwise isolate
the pathogen by inoculation of blood into susceptible animals if possible.
Animals. Inoculate blood or tissues into rats or mice.
PROGNOSIS:
Humans. The fatality rate is up to 40 per cent. Animals. Although
fatality is uncommon, the lesions tend to be progressive.
PREVENTION:
Humans and animals. Control tick vectors and prevent tick bites.
TREATMENT:
Humans. A single dose of tetracycline or erythromycin, 0.5 g orally,
or a single dose of procaine penicillin G, 600,000 units intramuscularly,
probably constitutes adequate treatment for louse-borne relapsing fevers.
Because of higher relapse rates, tick-borne disease is treated with 0.5
g of tetracycline or erythromycin given 4 times daily for 5-10 days. Jarisch-Herxheimer
reactions may occur and respond to aspirin given every 4 hours. Pretreatment
with steroids is not effective in preventing this reaction. Animals. Tetracycline,
penicillin, erythromycin, and ceftriaxone at standard dosages for 21-28
days.
LEGISLATION:
Humans.Louse-borne relapsing fever is notifiable to the World Health
organization. Tick-borne infection may be notifiable in some countries (e.g.
the UK). Animals.None.
LYME DISEASE
U.S. Centers for Disease Control and Prevention: Division of Vector-Borne
Infectious Diseases
Lyme Disease: Home Page
Disease Overview: Institutional Animal Care
and Use Committee, University of California, Santa Barbara.
(Lyme arthritis, Bannworth's syndrome, tick-borne meningopolyneuritis,
erythema chronicum migrans [ECM], Steere's disease)
AGENT:
Spirochete, Borrelia burgdorferi
RESERVOIR
AND INCIDENCE
First implicated in 1982 as agent in a 1975 epidemic of juvenile
inflammatory arthropathy in Old Lyme Connecticut. Cases have been reported
from 46 states and the annual number of Lyme disease cases has increased 18
fold from 497 to 8803. It is now the most common tick transmitted disease
in the USA. Also seen in Europe, England, Soviet Union, China, Japan, Southeast
Asia, South Africa, Australia, and Canada.
TRANSMISSION:
Transmitted mostly by Ixodes dammini and other ixodid ticks (three
host tick with a two to three year life cycle). Ixodes dammini has a broad
range of hosts; adults prefer white tailed deer but will also parasitize dogs,
horses, and humans. Larvae feed primarily on rodents, especially mice. Nymphs
feed on all hosts and appears to be primarily responsible for transmission
of the disease to people. Birds are an important reservoir and means of
dispersal. Also found in Dermacentor, Rhipicephalus and Amblyomma and other
ticks and biting insects, including mosquitoes, fleas, and biting flies.
Because of lack of any proof to the contrary it is generally believed at
this time that any potential increased risk to human beings from infected
animals is attributable to animals bringing ticks into areas of human habitation
rather than any pet transmission. Dogs appear to be at greater risk than
humans.
DISEASE
IN ANIMALS:
Serologic evidence has been reported in the dog, cat, horse, and
ruminants. However, correlation with disease is lacking except in the dog.
The dog exhibits the same symptoms as noted below for humans. Expanding skin
lesions have been noted in mice and rabbits.
DISEASE
IN MAN:
Multisystemic disease which may have chronic sequelae; an annular
rash known as erythema chronicum migrans (ECM) develops in 60-80% of patients
in the area of the tick bite and is considered pathognomonic. Also flu like
symptoms, which resolve in about three weeks. 8-10% of people develop cardiac
involvement several weeks later. Manifestations include atrioventricular
block, cardiomyopathy, heart failure, myocarditis, and pancarditis. 15% develop
neurologic disorders such as facial nerve palsies which usually resolve. Other
manifestations include meningitis, cranial neuritis, radiculoneuritis, neuropathy,
and encephalopathy. 60% develop the most common sequelae, arthritis. Disease
may remain latent with symptoms developing 4 years after seroconversion.
DIAGNOSIS:
Most common test is detecting antibody titers by IFA or ELISA (on
blood, CSF or synovial fluid). Culture is definitive but is difficult and
requires special media such as Barbour-Stoener-Kelly media. Histologically
with Dieterle Silver Stain or immunoperoxidase stains, but is often unrewarding.
TREATMENT:
A positive serology is no grounds for treatment when no clinical
signs are present. Borrelia burgdorferi is sensitive to tetracycline and moderately
sensitive to penicillin. amoxicillin, ceftriaxone, and imipenem are also
highly active.
PREVENTION\CONTROL:
Tick control care when removing ticks or when handling potentially
infective materials a vaccine against Lyme Disease tested in hamsters has
been found effective. More research is needed but in the future vaccination
may be beneficial for those at constant risk of exposure.
ZOONOTIC DISEASES
ENTERIC INFECTIONS
CAMPYLOBACTERIOSIS
Centers for Disease Control and Prevention: National Center for
Infectious Diseases
Campylobacteriosis
Disease Overview: Institutional Animal Care
and Use Committee, University of California, Santa Barbara.
(Vibriosis, vibrionic abortion)
AGENT:
Campylobacter (Vibrio) fetus ss. jejuni, a gram negative, microaerophilic,
curved, motile rod that is worldwide in distribution.
RESERVOIR
AND INCIDENCE
Isolated from laboratory animals including dog, cat, hamsters,
ferrets (>60 % in one study), nonhuman primates, rabbits, swine, sheep,
cattle, and birds Although most cases of human campylobacteriosis are of unknown
origin, infection after contact with sick animals has been well documented.
*In most reports of pet to human transmission of C. jejuni, diarrheic puppies
or kittens from pounds have been the source of infection. Pet birds, chickens,
and kittens are implicated in other reports. A lab animal technician developed
Campylobacter enteritis after feeding and cleaning up after a recently imported
nonhuman primate. The organism was first isolated from nonhuman primates from
Macaca fascicularis in 1979 and has since been reported in baboons, rhesus,
patas, and marmosets. Can be shed for long periods of time in stool by asymptomatic
carriers. Younger animals seem more likely to acquire the infection and hence
may more commonly shed the organism.
TRANSMISSION:
Transmission is thought to occur by the fecal-oral route, through
contamination of food or water, or by direct contact with infected fecal material.
The organism has also been isolated from houseflies. At 40 C the organism
is viable for three weeks in feces and milk, four weeks in water, and five
weeks in urine. Campylobacter is shed in the feces for at least six weeks
after infection. Infected children may transmit infection to puppies or kittens,
which may then expose other children. Poultry and cattle are the main reservoirs
for human infection, which is acquired by ingesting contaminated raw milk,
undercooked chicken or other food contaminated in the kitchen.
DISEASE
IN NONHUMAN PRIMATES:
Variable. the majority are asymptomatic carriers. Mild to severe
enteritis may be seen accompanied by fever, vomiting, and mucus and blood
in the feces. Bacteremia may occur complicated by meningitis or abortion.
Most signs appear 1 to 7 days after exposure and affect primarily the jejunum,
ileum, and colon.
DISEASE
IN FERRETS:
Asymptomatic to proliferative colitis. Shed organisms for long
period of time (> 16 weeks).
DISEASE
IN OTHER ANIMALS:
Has also been shown to cause hepatitis in poultry, proliferative
ileitis in hamsters, and abortion in ruminants. In all animals, it may be
associated with diarrhea, especially when acting secondarily to virus infection.
DISEASE
IN MAN:
Acute gastrointestinal illness, diarrhea with or without blood,
abdominal pain, and fever. It may cause pseudoappendicitis and, rarely, septicemia
and arthritis. Usually a brief, self-limiting disease. In humans the asymptomatic
carrier state is rare. Reinfection is possible in both animals and man.
DIAGNOSIS:
1. Rapid diagnosis is done with dark field or phase contrast microscopy
of fecal material. 2. This is confirmed by stool culture which requires a
special selective growth media(CAMPY-BAP) and incubation at 43oC with 10%
CO2, 5% O2 and 85% Nitrogen. 3. Warthin Starry stain and histo 4. Various
techniques are being used to detect seroconversion to the antigens of Campylobacter.
TREATMENT:
Animals can be treated based on culture and sensitivity. Currently
erythromycin is the drug of choice, but does not eliminate the carrier state.
Tetracycline or ciprofloxacin are alternatives.
PREVENTION\CONTROL:
Vaccines provide partial protection of short duration and routine
use is not recommended. Control is aimed at isolation of affected individuals
and personal hygiene. An increased awareness of the potential of infection
due to Campylobacter is of primary importance. Thoroughly cook all foodstuffs
derived from animal sources, particularly poultry. Recognize, prevent, and
control Campylobacter infections among domestic animals and pets. Wash hands
after handling poultry and animal feces.
COLIBACILLOSIS
Disease Overview: Institutional Animal Care
and Use Committee, University of California, Santa Barbara.
(Colibacteriosis, colitoxemia, white scours, gut edema of swine)
AGENT:
Escherichia coli are gram-negative, aerobic, and facultatively
anaerobic medium-sized rods.
RESERVOIR
AND INCIDENCE
Worldwide; some endemic areas exist in developing countries.
TRANSMISSION:
Some serotypes are species-specific, others are not. Milk, milk
products, and meat products can contain pathogenic serotypes. Foods of animal
origin and contact with dogs and cats have been indicated as sources of infection
for children.
DISEASE
IN ANIMALS:
Calf diarrhea (white scours) is an acute disease causing mortality
in calves less than 10 days old. It manifests itself as serious diarrhea,
with whitish feces and rapid dehydration. Mastitis caused by E. coli appears
especially in older cows with dilated milk ducts. A long-term study of horse
fetuses and newborn colts found that close to 1% of abortions and 5% of deaths
of newborns were due to E. coli. Neonatal enteritis caused by E. coli in
suckling pigs begins 12 hours after birth with a profuse watery diarrhea,
and may end with fatal dehydration. Edema in suckling pigs (gut edema) is
an acute disease that generally attacks between 6 and 14 weeks of age. It
is characterized by sudden onset, incoordination, and edema of the eyelids,
the cardiac region of the stomach, and sometimes other parts of the body.
During septicemic diseases of fowl, such as cases of salpingitis and pericarditis,
pathogenic serotypes of E. coli have been isolated. A colibacillary etiology
has also been attributed to Hjarre's disease (coligranuloma), which is a
condition in adult fowl characterized by granulomatous lesions in the liver,
cecum, spleen, bone marrow, and lungs.
DISEASE
IN HUMANS:
The enterotoxigenic stains (ETEC) cause profuse and watery diarrhea,
abdominal colic, vomiting, acidosis, and dehydration. Enteroinvasive strains
cause a dysenteric syndrome with mucoid diarrhea, at times tinged with blood.
E. coli is also an important agent of urogenital infections.
DIAGNOSIS:
Stool culture or immunoassays for enterotoxins.
TREATMENT:
Ciprofloxacin or trimethoprim-sulfa.
PREVENTION/CONTROL:
With respect to man, control measures include: a) personal cleanliness
and hygienic practices, sanitary waste removal and b) protection of food products.
Vaccines for swine and bovine have been developed.
SALMONELLOSIS
Centers for Disease Control and Prevention: National Center for
Infectious Diseases
Salmonellosis
Disease Overview: Institutional Animal Care
and Use Committee, University of California, Santa Barbara.
(Enteric paratyphosis)
AGENT:
Gram negative bacteria. Out of 1600 recognized serotypes of Salmonella,
S. typhimurium & S. enteritidis have been associated most commonly with
lab animal colony infections. In the U.S., 5 million cases are diagnosed annually.
S. typhi, the cause of Typhoid Fever, rarely occurs in the U.S. and is not
discussed here.
RESERVOIR
AND INCIDENCE
The organism inhabits the intestinal tract of many animals including
birds, cattle, sheep, pigs, lab. animals (rats, mice, hamsters, guinea pigs,
nonhuman primates) and humans. Salmonella occurs worldwide. *The house mouse
may also be a reservoir of the infection and may play a role in human and
animal salmonellosis. Humans, rarely, and animals may be carriers and asymptomatic
shedders of the organism. *Salmonella prevalence in the U.S. canine population
may be 10% or more. *Prevalence data from 8 studies conducted worldwide
indicated that a wide range (0.6-27%) of cats were culture-positive for Salmonella.
*Salmonella carriers in newly imported Rhesus and Cynomolgus monkeys exceeded
20% in some shipments. *Birds, reptiles, and turtles are especially dangerous
sources of Salmonellosis. 94% of all reptiles harbor Salmonella. Turtles alone
in 1970 may have caused 280,000 human cases of Salmonellosis. *In 1975 the
FDA ruled it illegal to sell a. Viable Turtle eggs b. Live turtles with a
carapace length < 10.2cm (4 inches) c. Exceptions - Educational & scientific
institutions and marine turtles. d. Marine turtles have not been shown to
be a reservoir of Salmonella THERE WAS A 77% DECREASE IN TURTLE ASSOCIATED
SALMONELLOSIS AFTER ENACTMENT OF THIS LAW.
TRANSMISSION:
Indirect transmission via contaminated food and water are the most
common sources but transmission may also be by direct contact. It is a common
contaminant of sewage. Found in many environmental water sources. Environmental
contamination continues to be a potential source of infection for lab animals
and secondarily for personnel handling those animals. *Animal feed containing
animal by products continues to be a source of Salmonella contamination,
especially if the diets consist of raw meal and have not undergone the pelleting
process.
DISEASE
IN ANIMALS:
Can be asymptomatic with clinical signs precipitated by stress;
penetration of the infection into the mucosa is followed by inflammation,
especially ileitis, progressing to inflamed mesenteric lymph nodes in the
mesentery, possibly progressing to septicemia and pneumonia especially in
calves. Calves undergo epizootic outbreaks of diarrhea with high mortality.
Abortion in cattle is caused by massive proliferation of salmonella in the
placenta leading to placental necrosis. High percentage of survivors become
carriers. Infected sheep, goats, and poultry usually show no signs of infection.
DISEASE
IN MAN:
Acute gastroenteritis with sudden onset of abdominal pain, diarrhea,
nausea, and fever. May lead to septicemia. May be an inapparent infection.
DIAGNOSIS:
Fecal Culture with selective media. Can get false negatives, though
because organism is shed intermittently. In the carrier state bacterium resides
in the gall bladder (NHP).
TREATMENT:
Symptomatic. Severely ill patients are treated with trimethoprim-sulfamethoxazole,
ampicillin, or ciprofloxacin.
PREVENTION\CONTROL:
Rapid detection and treatment (acute and chronic) in lab animals.
Treatment based on culture and sensitivity. Cull carrier animals. Watch during
quarantine period. Sanitation and hygiene, protective clothing, gloves Rodent,
bird & wild animal control is important. Examine feed and bedding and
pasteurize or autoclave, if necessary. Consider screening animal care personnel
for inapparent Salmonella infection to prevent the introduction of Salmonella
into the colony from infected workers. Thoroughly cook all foodstuffs derived
from animal sources. Exclude animal care personnel with diarrhea.
STAPHYLOCOCCAL FOOD POISONING
Disease Overview: Institutional Animal Care
and Use Committee, University of California, Santa Barbara.
(Staphylococcal Alimentary Toxicosis, Staphylococcal Gastroenteritis)
AGENT:
Coagulase-positive strains of Staphylococcus aureus, a gram-positive
cocci.
RESERVOIR
AND INCIDENCE
Worldwide. The principle reservoir is the human carrier. Infected
cows, fowls, and dogs may give rise to and be a source of staphylococcal poisoning
in man.
TRANSMISSION:
A high proportion of healthy humans (30-35%) have staphylococci
in the nasopharynx and on the skin. Sneezing, coughing, expectorating can
contaminate food. Similarly, he may contaminate foods handled if he has a
skin lesion. Milk from cow udders infected can contaminate numerous milk products.
Contaminated egg contents can also be a source of infection.
DISEASE
IN ANIMALS:
Mastitis in cattle. Pyoderma, impetigo, folliculitis, and furunculosis
in dogs. In fowl, staphylococcal infection can cause diseases ranging from
pyoderma to septicemia with different locations (salpingitis, arthritis,
and other disorders).
DISEASE
IN HUMANS:
The major symptoms are nausea, vomiting, abdominal pains, and diarrhea.
It is the cause of toxic shock syndrome in women.
DIAGNOSIS:
Culture of vomitus, feces, or a suspected food item.
TREATMENT:
Electrolyte and fluid replacement. Ciprofloxacin.
PREVENTION/CONTROL:
Reduce food handling time. Exclude persons with boils, abscesses,
and other purulent lesions from handling food. Educate food handlers in strict
food hygiene.
ANTHRAX
Centers for Disease Control and Prevention: National Center for
Infectious Diseases
Anthrax
(Bacillus anthracis infection)
Office International des Epizooties
Anthrax:
Manual of standards Diagnostic Tests and Vaccines 2000
Disease Overview: Institutional Animal Care
and Use Committee, University of California, Santa Barbara.
(Malignant pustule, wool-sorters' disease, charbon, malignant edema,
splenic fever) An acute bacterial infection of humans and animals which may
be rapidly fatal. The disease occurs worldwide and is enzootic in certain
African and Asian countries. It is an occupational hazard of persons such
as wool-sorters, fellmongers, knackermen, farm workers and veterinarians in
contact with infected animals or their products (e.g., blood, wool, hides
and bones). The causative agent is Bacillus anthracis (bacterium).
RESERVOIR
AND MODE OF TRANSMISSION:
All domestic, zoo and wild animals are potentially at risk of infection.
Anthrax bacilli are released from infected carcasses and form resistant spores
on exposure to air. These spores contaminate soil for many years. Humans
are usually infected by inoculation from direct contact with infected animals,
carcasses or animal products and contaminated soil. Inhalation or ingestion
of spores may occur. Animals are infected from contaminated feed, forage,
water or carcasses. Laboratory accidents have occurred.
INCUBATION
PERIOD:
Humans. Cutaneous 3-10 days inhalation 1-5 days gastrointestinal
2-5 days. Animals. 1-5 days.
CLINICAL
FEATURES:
Humans. Various forms include: 1. Cutaneous anthrax; localized
ulceration and scab with fever and headache which may be followed within a
few days by septicemia and meningitis. 2. Inhalation anthrax; fulminating
pneumonia. 3. Intestinal anthrax; acute gastroenteritis with bloody diarrhoea.
Animals. Peracute cases are found dead or moribund. Acute cases show fever,
excitation followed by depression, incoordination, convulsion and death. Chronic
cases show edema of throat, pharynx and brisket, especially in pigs.
PATHOLOGY:
Humans. Features include black scab (eschar) with edema, enlargement
of regional lymph nodes and possibly septicemia; pneumonia and generalized
hemorrhages. Animals. Carcasses should not be opened, hence necropsy is
rarely carried out. Main features include failure of the blood to clot and
hemorrhages throughout the body. The spleen is enlarged and softened. The
subcutaneous swelling, mainly about the neck and throat of affected pigs
and horses, contains gelatinous fluid. The blood contains very large numbers
of B. anthracis.
DIAGNOSIS:
Humans. Identify B. anthracis in stained blood smears or by inoculation
of laboratory animals. Culture swabs from wounds. Animals. As for humans.
Specific antigen for anthrax may be found in animal products (e.g. hides)
using a precipitin (Ascoli) test.
PROGNOSIS:
Humans. Untreated cutaneous anthrax has a fatality rate of 5-20
Per cent and gastrointestinal anthrax of 25-75 per cent. Pulmonary anthrax
is usually fatal. Animals. The condition is usually fatal in cattle unless
treated early. Pigs and horses are more resistant.
PREVENTION:
Humans. Prohibit contact with infected animals and their products.
Establish environmental and personal hygiene (e.g., ventilation and protective
clothing) where a special risk exists. Treat wounds promptly and disinfect
imports of hairs and wool. Vaccination may protect those occupationally exposed
to risk. Apply strict laboratory safety measures. Isolate infected patients,
with concurrent disinfection. Animals. Sterilize, or avoid using, meat and
bone meal from high-risk countries for animal feed. Vaccinate livestock
grazing in enzootic area. Dispose of infected carcasses safely and fence
off areas contaminated by inadequately buried carcasses.
TREATMENT:
Humans. The mortality rate is high despite proper therapy, especially
in pulmonary disease. Penicillin G, 2 million units IV every 4 hours, is the
therapy of choice. tetracycline, 500 mg orally every 6 hours, may be used
for mild, localized cutaneous infection. Animals. Penicillin injection of
all animals showing fever after the first case is confirmed. This involves
checking temperatures twice daily.
VACCINATION:
Humans. Offered to workers at risk. Animals. Non-encapsulated Stern
strain vaccine can be used in all species of domestic animal. Annual vaccination
of grazing animals using spore or alum precipitated antigen vaccine in areas
of high risk is recommended.
LEGISLATION:
Humans. The disease is notifiable in most countries. It is a recognized
occupational disease in some countries, including the UK. Animals. Notifiable
in many countries with mandatory disposal of infected carcasses by burning
or deep burial under lime. Opening of moving suspect carcasses is prohibited.
STAPHYLOCOCCAL FOOD POISONING
Disease Overview: Institutional Animal Care
and Use Committee, University of California, Santa Barbara.
SYNONYMS:
Staphylococcal alimentary toxicosis, staphylococcal gastroenteritis.
ETIOLOGY:
Coagulase-positive strains of Staphylococcus aureus that produce
enterotoxins. Very few coagulase-negative stains are enterotoxigenic. The
toxin is preformed in the food involved. To date, six types of enterotoxins
are known: A, B, C, D, E, and F; of these A is the most prevalent in outbreaks.
Enterotoxin F is implicated in toxic shock syndrome (TSS). Some strains can
produce two or even three different enterotoxins. The toxins are heat-resistant
and can withstand a temperature of 100oC for 30 minutes.
GEOGRAPHIC
DISTRIBUTION:
Worldwide.
THE DISEASE
IN MAN:
The incubation period is short, generally 3 hours after ingestion
of the food involved. The interval between consumption of the enterotoxin
and the first symptoms can vary from 30 minutes to 8 hours, depending on the
quantity of toxin ingested and the susceptibility of the individual. The
major symptoms are nausea, vomiting, abdominal pains, and diarrhea. Some patients
may show low pyrexia (up to 38oC). More serious cases manifest prostration,
cephalalgia, abnormal temperature, and lowered blood pressure, as well as
blood and mucus in the stool and vomit. The course of the disease is usually
benign and the patient recovers without medication in 24 to 72 hours. Recently,
a toxic shock syndrome has been described. Symptoms consist of vomiting,
diarrhea, high fever, erythroderma, edema, renal insufficiency, and toxic
shock. Most patients are women who become ill during their menstrual period.
The above-described symptoms also are observed in association with abscesses
and osteomyelitis caused by S. aureus. A staphylococcal enterotoxin designated
F was isolated from 94% of these patients strains of S. aureus from nine
patients with toxic shock were examined, and production of enterotoxin F
was confirmed in eight of them; only 42% of 50 strains isolated from other
hospitalized patients produced this toxin. Toxin F production was not found
in 48 strains originating from animal clinical specimens. Of 24 strains from
healthy human carriers, 25% produced the toxin.
SOURCE
OF INFECTION AND MODE OF TRANSMISSION:
The principal reservoir of is S. aureus is the human carrier. A
high proportion (from 30 to 35%) of healthy humans have staphylococci in the
nasopharynx and on the skin. A carrier with a respiratory disease can contaminate
foods by sneezing coughing, or expectorating. Similarly, he may contaminate
foods he handles if he has a staphylococcal skin lesion. However. even if
not sick himself, the carrier may spread the agent by handling food ingredients.
utensils, and equipment. or the finished food product. According to different
authors, the proportion of enterotoxin-producing S. aureus strains of human
origin varies between 18 and 75%. The proportion of toxigenic strains isolated
from various sources (human, animal, and food) is very high. Strains of human
origin predominate in epidemics, but animals are also reservoirs of the
infection. Milk from cow udders infected with staphylococci can contaminate
numerous milk products. Many outbreaks have been produced by consumption of
inadequately refrigerated raw milk or cheeses from cows whose udders harbored
staphylococci. The largest outbreak affected at least 500 students in California
between 1977 and 1981 and was traced to chocolate milk. In developing countries,
where refrigeration after milking is often inadequate, milk and milk products
may be an important source of staphylococcal intoxication. According to recent
investigations, a high proportion of strains isolated from staphylococcal
mastitis produce enterotoxin A, which causes many outbreaks in humans. In
several investigations it was possible to isolate from skin lesions and cow's
milk the S. aureus phage type 80/81, which is related to epidemic infections
in man. One of the studies proved that phage type 80/81 produced interstitial
mastitis in cows. The same phage type was found among animal caretakers, which
indicates that the bacterium is intertransmissible between man and animals
and that the latter may reinfect man. Infected fowl and dogs may also give
rise to and be a source of staphylococcal poisoning in man. One subject that
deserves special attention is the appearance of antibiotic-resistant strains
in animals whose food includes antibiotics. Concern exists over the possible
transmission of these strains to man. On several occasions, resistant stains
have been found both in animals (cows, swine, and fowl) and in their caretakers,
with the same antibiotic resistance. Moreover, "human" strains (phage typed)
have on occasion been isolated from the nostrils and lesions of other species
of domestic animals. A variety of foods and dishes may be vehicles of the
toxin. If environmental conditions are favorable, S. aureus multiplies in
the food and produces enterotoxins. Once made, the toxin is not destroyed
even if the food is subjected to boiling while being cooked. Consequently,
the toxin may be found in the food whereas staphylococci are not. An important
causal factor in food-borne intoxications is holding food at room temperature,
which permits multiplication of staphylococci. Lack of hygiene in food handling
is another notable factor. Frequently, outbreaks of food poisoning may be
traced to a single dish.
THE ROLE
OF ANIMALS IN THE EPIDEMIOLOGY OF THE DISEASE:
Most outbreaks are caused by human strains, and to a lesser degree
by strains from cattle and other domestic animals. Animal products -- such
as meat, ham, milk, cheese, cream, and ice cream -usually constitute a good
substrate for staphylococcal multiplication. Milk pasteurization offers no
guarantee of safety if toxins were produced before heat treatment, as the
toxins are heat-resistant. Outbreaks have been caused by reconstituted powdered
milk, even when the dried product contained few or no staphylococci.
DIAGNOSIS:
The short incubation period between ingestion of contaminated food
and appearance of symptoms is the most important clinical criterion. Laboratory
confirmation, when possible, is based above all on demonstration of the presence
of enterotoxin in the food. Biological methods (inoculation of cats with
cultures of the suspect food, or of rhesus monkeys with the foodstuffs or
cultures) are expensive and not always reliable. As substitutes, serologic
methods such as immunodiffusion, immunofluorescence, hemagglutination inhibition,
and, recently, ELISA are increasingly used. In febrile patients, blood cultures
are indicated. Isolation of enterotoxigenic staphylococcal strains from foods
and typing by phage or, more recently, by immunofluorescence have epidemiologic
value. Quantitative examination of staphylococci in processed or cooked
foods serves as an indicator of hygienic conditions in the processing plant
and of personnel supervision.
TREATMENT:
In humans, treatment usually consists of replacement of fluids
and electrolytes and, very rarely, management of hypovolemic shock and respiratory
embarrassment. If botulism is suspected, polyvalent antitoxin must be administered.
Historically, antimicrobial drugs have not been recommended unless a specific
microbial agent producing progressive systemic involvement can be identified.
Preliminary data now suggest that ciprofloxacin, 500 mg every 12 hours for
5 days, may shorten the duration of diarrhea and lead to a more rapid resolution
of symptoms. Antimotility drugs may relieve cramping and decrease diarrhea
in mild cases. Their use should be limited to patients without fever and
without dysentery (bloody stools), and they should be used in low doses.
CONTROL:
It includes the following measures: a) education of persons who
prepare food at home or commercially in proper personal hygiene; b) exclusion
from handling food of individuals with abscesses or other skin lesions; and
c) refrigeration of all foods to prevent bacterial multiplication and formation
of toxins. Foods should be kept at room temperature as little time as possible.
The veterinary milk inspection service should supervise dairy installations,
ensuring that refrigeration units function correctly and are used immediately
after milking, and that milk is refrigerated during transport to pasteurization
plants. The veterinary meat inspection service should be responsible for
enforcing hygienic regulations before and after slaughter as well as during
handling and production of meat products. Control of hygienic conditions
in meat retail establishments ts also important.
LEPROSY
Centers for Disease Control and Prevention: Division of Bacterial
and Mycotic Diseases
Hansen's
Disease (Leprosy)
Disease Overview: Institutional Animal Care
and Use Committee, University of California, Santa Barbara.
(Hansen's disease)
AGENT:
Mycobacterium leprae, a polymorphic acid-fast bacillus.
RESERVOIR
& INCIDENCE:
The world prevalence is estimated to be between 10 and 12 million.
Newly recognized cases in the USA are diagnosed principally in California,
Hawaii, Texas, Florida, Louisiana, and New York City, and in Puerto Rico.
Most of these cases are in immigrants and refugees whose disease was acquired
in their native country; however, the disease remains endemic in Hawaii, Texas,
California, Louisiana and Puerto Rico. Man is the only significant reservoir.
Armadillos, mangabey monkeys, and chimpanzees can acquire the disease from
humans. Epidemiologic data on leprosy in the U.S. reveal very high ratios
of native to foreign-born leprosy patients in Texas and Louisiana in comparison
to all other states. These are the 2 states known to have the highest prevalences
of leprosy in wild armadillos.
TRANSMISSION:
Respiratory and involves prolonged exposure in childhood. Only
rarely have adults become infected.
DISEASE
IN ANIMALS:
The disease in armadillos (Dasypus novemcinctus) is similar to
the lepromatous form in man. Infection in these animals is characterized by
macrophage infiltrates containing a large number of bacilli. M. leprae is
known to prefer the coldest parts of the human body. For this reason, armadillos
are used as experimental animals since their body temperature is 30-35oC.
In chimpanzees, the disease appears as a progressive chronic dermatitis with
nodular thickening of the skin of the ears, eyebrows, nose, and lips. Sooty
mangabey monkeys develop lepromatous leprosy with neuropathic deformities
of the extremities, including clawing of the digits.
DISEASE
IN HUMANS:
In lepromatous leprosy, nodules, papules, macules and diffuse infiltrations
are bilaterally symmetrical and usually numerous and extensive; involvement
of the nasal mucosa may lead to crusting, obstructed breathing and epistaxis;
ocular involvement leads to iritis and keratitis. In tuberculoid leprosy,
skin lesions are single or few, sharply demarcated, anesthetic or hyperesthetic,
and bilaterally asymmetrical; peripheral nerve involvement tends to be severe.
DIAGNOSIS:
Demonstration of acid-fast bacilli from skin or nasal septum scrapings.
TREATMENT:
Combination therapy is recommended since single-drug treatment
is accompanied by emergence of resistance. Lepromatous leprosy is treated
with dapsone, clofazimine, and rifampin. Tuberculoid leprosy is treated with
dapsone and rifampin.
PREVENTION/
CONTROL:
Early detection and treatment. Contact isolation for lepromatous
leprosy but not necessary for tuberculoid leprosy.
DERMATOPHILOSIS
Office International des Epizooties
Dermatophilosis:
Manual of standards Diagnostic Tests and Vaccines 2000
Disease Overview: Institutional Animal Care
and Use Committee, University of California, Santa Barbara.
(Streptotrichosis, Mycotic Dermatitis of Sheep)
AGENT:
Dermatophilus congolensis. An aerobic actinomycete with gram positive
long branching filaments and coccoid bodies.
RESERVOIR
AND INCIDENCE
Occurs in temperate regions worldwide. Natural disease described
in horses, cattle, sheep, goats, cottontail rabbits, owl monkeys, lizards
& humans.
TRANSMISSION:
The etiologic agent is an obligate parasite that has been isolated
only from lesions in animals. Human cases have arisen from direct contact
with infected animals. The most common means of transmission between animals
is mechanical thru arthropod vectors. The infection may also be transmitted
by means of objects, such as plant thorns or shears.
DISEASE
IN ANIMALS:
Circumscribed areas of alopecia, elevated crusty papillomatous
lesions, and exudative dermatitis. **Owl monkeys may have relapsing Dermatophilosis
after apparently appropriate antibiotic regimens. Therefore organism may persist
on pelage of animals after resolution of lesions. In cats, the lesions differ
from those of other domestic animals by affecting deeper tissues. In cats,
granulomatous lesions have been found on the tongue, bladder, and popliteal
lymph nodes.
DISEASE
IN MAN:
Pustular desquamative dermatitis.
DIAGNOSIS:
Microscopic exam of stained material from lesions and culture.
PREVENTION\CONTROL:
1. Treatment with antibiotics 2. Isolate affected animals 3. Protective
clothing, gloves, personal hygiene 4. Tick control.
ERYSIPELOID
Disease Overview: Institutional Animal Care
and Use Committee, University of California, Santa Barbara.
(Rosenbach's erysipeloid, erythema migrans, erysipelotrichosis,
rose disease in swine, diamond skin disease in swine, fish-handler's disease
or fish rose in man).
AGENT:
Erysipelothrix rhusiopathiae (insidiosa). 22 different serotypes
are recognized. *Discovered by ROBERT KOCH==He called it the Bacillus of Mouse
Septicemia.
RESERVOIR
AND INCIDENCE
Saprophyte in soil, water, and decaying organic matter. Pathogen
in swine, lambs, calves, poultry, fish, & wild and lab mice. *Pigs probably
represent the most likely source of exposure in the laboratory environment.
(Natural disease or zoonotic transmission from lab rodents has NOT been
reported.)
TRANSMISSION:
Contamination of wounds while handling infected tissues.
DISEASE
IN ANIMALS:
Diamond skin disease in pigs. Arthritis in sheep and swine. Cyanosis
and hemorrhages in turkeys. Can be septicemic disease in many species.
DISEASE
IN MAN:
Disease in humans is called Erysipeloid, and is primarily occupation
related. Inflammatory lesions of the skin, with elevated erythematous edge;
spreads circumferentially. Septicemia is an infrequent complication.
DIAGNOSIS:
Culture from lesion or blood.
PREVENTION\CONTROL:
Treatment with Penicillin Gloves when handling animals Vaccine
for swine and turkeys.
MELIOIDOSIS
Centers for Disease Control and Prevention: Division of Bacterial
and Mycotic Diseases
Melioidosis
(Burkholderia pseudomallei)
Disease Overview: Institutional Animal Care
and Use Committee, University of California, Santa Barbara.
(Pseudoglanders, Whitmore's disease)
AGENT:
Pseudomonas pseudomallei (Malleomyces pseudomallei, Actinobacillus
pseudomallei ) --MOTILE, Gram negative rod.
RESERVOIR
AND INCIDENCE
Normal inhabitant of surface soil and water in Southeast Asia,
and tropical areas. Recent studies have shown that the water of tanks in which
exotic aquarium fishes were imported was contaminated. Occurs in wild rodents,
goats, pigs, sheep. Also identified in Chimps, orangutans, and macaques. There
is no evidence that animals are important reservoirs, except in the transfer
of the agent to new foci. Rare in the U.S. except in drug users.
TRANSMISSION:
By inhalation from moist soil-water reservoir, by contact with
contaminated soil or water thru overt or inapparent skin wounds, or by ingestion
of contaminated feeds. Can be venereal in man.
DISEASE
IN ANIMALS:
Signs include loss of weight, swelling of joints, fever, cough,
and chest pain. Skin lesions with fistulous tracks can develop. Emaciation
and multiple abscesses in lung, bone, viscera. A chronic draining purulent
skin lesion in a primate is suspect. Incubation period can be 6 months to
three years. Sheep seem especially susceptible- over 25% mortality can occur
in outbreaks.
DISEASE
IN MAN:
Clinical disease is not common in man but subclinical disease in
endemic areas based on serology is common. It may simulate typhoid fever or
TB including pulmonary cavitation, empyema, chronic abscesses and osteomyelitis.
High case fatality rate (80%) in people who do develop clinical signs.
DIAGNOSIS:
Culture and isolation from lesions, a rising serological titer
is confirmatory.
TREATMENT:
ceftazidime. Alternates: Chloramphenicol or Trimethoprim-sulfamethoxazole.
CONTROL:
Safe disposal of sputum and wound discharges.
GLANDERS
Office International des Epizooties
Glanders:
Manual of standards Diagnostic Tests and Vaccines 2000
Disease Overview: Institutional Animal Care
and Use Committee, University of California, Santa Barbara.
(Farcy)
AGENT:
Pseudomonas mallei (Actinobacillus mallei) NONMOTILE, gram negative
rod
RESERVOIR
AND INCIDENCE
Disease of equidae and rarely man. Occasionally reported in dogs,
cats, sheep, and goats. Mostly seen in Asia and Mediterranean areas, rare
in North America.
TRANSMISSION:
Spread by contamination by infectious discharges of wounds and
mucus membranes and by ingestion.
DISEASE
IN ANIMALS AND MAN:
Pulmonary form: cough, nasal discharge. cutaneous form: multiple,
purulent, cutaneous eruptions, often following lymphatics. Usually affects
hind legs of horses. May have long periods of remission. The fatality rate
in humans is 95% if left untreated. Horses usually suffer chronic and sometimes
fatal illness. Asses and mules usually suffer acute disease which is often
fatal.
DIAGNOSIS:
Cannot be differentiated from P. pseudomallei serologically. Specific
diagnosis can be made only by characterization of the isolated organism.
TREATMENT:
Streptomycin + tetracycline or chloramphenicol + streptomycin.
PREVENTION/CONTROL:
1. Treatment with antibiotics 2. Elimination of carrier animals
3. Gloves, protective clothing when handling infected animals.
TULAREMIA
Centers for Disease Control and Prevention: National Center for
Infectious Diseases
Tularemia
(Francisella tularensis Infection)
Office International des Epizooties
Tularemia:
Manual of standards Diagnostic Tests and Vaccines 2000
Disease Overview: Institutional Animal Care
and Use Committee, University of California, Santa Barbara.
(Francis' disease, deer-fly fever, rabbit fever, O'Hara disease)
AGENT
Francisella tularensis, a small pleomorphic, gram-negative, nonmotile
rod or coccobacillus that can survive several weeks in the external environment.
RESERVOIR
AND INCIDENCE
Common often fatal septicemic disease of rabbits, squirrels, muskrats,
deer, bull snakes, sheep, wild rodents, cats and dogs. Major reservoirs are
RABBITS, TICKS, MUSKRATS. Has been reported in NHP's at an urban zoo. Natural
infection in laboratory animals and zoonotic transmission from them has
NOT been reported.
TRANSMISSION:
Handling tissue of infected animals (direct contact with UNBROKEN
skin is sufficient). Reported human infections due to a cat bite and scratch
and a NHP bite also reported. transmitted by biting insects inhalation, ingestion.
DISEASE
IN ANIMALS:
Clinical signs usually occur alongside heavy infestation with ticks,
and include sudden high fever, anorexia and stiffness, eventually leading
to prostration and death. In sheep, pregnant ewes may abort. Affected dogs
have soft nodular swellings under the skin. Miliary foci of necrosis occur
in the liver, spleen and lymph nodes. Severe lesions in the lung involve widespread
consolidation with edema and pleurisy.
DISEASE
IN MAN:
Fever, headache, and nausea begin suddenly, and a local lesion-a
papule-develops and soon ulcerates. Regional lymph nodes may become enlarged
and tender and may suppurate. The local lesion may be on the skin of an extremity
(ulceroglandular disease) or in the eye. Pleuropulmonary disease may develop
from hematogenous spread or may be primary after inhalation. Following ingestion
of infected meat or water, an enteric (typhoidal) form may be manifested by
enteritis, stupor, and delirium. In any type of involvement, the spleen may
be enlarged and tender and there may be nonspecific rashes, myalgias, and
prostration. A case fatality rate of 5-10% mainly from the typhoidal or pulmonary
form exists.
DIAGNOSIS:
Culture (requires specialized laboratory and dangerous, therefore,
not recommended) A positive agglutination test (>1:80) develops in the
second week after infection and may persist for several years.
TREATMENT
IN MAN:
Streptomycin + tetracycline. Chloramphenicol may be substituted
for tetracycline.
PREVENTION\CONTROL:
Wear impervious gloves while handling animals or tissues cook the
meat of wild rabbits and rodents thoroughly vaccine available for high risk
personnel avoid bites of flies, mosquitos, and ticks and avoid drinking, bathing,
swimming in untreated water in endemic areas.
STREPTOCOCCOSIS
Centers for Disease Control and Prevention: National Center for
Infectious Diseases
Streptococcus
pneumoniae Infection
Disease Overview: Institutional Animal Care
and Use Committee, University of California, Santa Barbara.
AGENT:
The causative agents are various streptococci species, including
Streptococcus suis and S. zooepidemicus.
RESERVOIR
AND INCIDENCE
Pigs are the reservoir of S. suis.
TRANSMISSION:
Humans are infected with S. suis by handling infected meat. S.
zooepidemicus has occurred in persons in direct contact with domestic animals
and from drinking raw milk.
DISEASE
IN ANIMALS:
S. suis epizootics may occur in pigs with high mortality, heralded
by signs of meningitis including depression, fever, incoordination and paralysis.
Suppurative arthritis may occur. More usually the disease is subclinical.
S. zooepidemicus may cause mastitis in cattle.
DISEASE
IN MAN:
S. suis causes fever and occasionally meningitis. S. zooepidemicus
may cause upper respiratory tract symptoms, cervical adenitis, pneumonia,
endocarditis and nephritis. A fatality rate of 8% has been reported for S.
suis, with residual deafness in a high proportion of survivors.
DIAGNOSIS:
Isolation and culture.
TREATMENT:
Benzathine Penicillin G. For persons allergic to penicillin, erythromycin
is an effective alternative. However, increasing reports of resistance from
Europe threatens its clinical utility.
PREVENTION/CONTROL:
Exercise caution in handling pig meat. Dress all wounds to avoid
contamination. Pasteurize milk.
RAT BITE FEVER
Disease Overview: Institutional Animal Care
and Use Committee, University of California, Santa Barbara.
(Streptobacillary fever, Haverhill fever, epidemic arthritic erythema,
sodoku)
AGENT:
Gram negative, pleomorphic bacillus. Two different agents can cause
disease: 1. Streptobacillus moniliformis (Haverhill Fever) *Named after a
1926 outbreak in Haverhill, Mass. attributed to contaminated milk. 2. Spirillum
minus (Sodoku).
RESERVOIR
AND INCIDENCE
Present in the oral and respiratory passages of a large number
of asymptomatic rodents, including Rats and Mice. Incidence of disease appears
to be low. Historically, wild rat bites and subsequent illness (usually small
children) relate to poor sanitation and overcrowding.
TRANSMISSION:
Man infected by bite of infected rodent or via contaminated milk
or food.
DISEASE
IN ANIMALS:
Rats: inapparent infection Mice: acute, systemic, fatal disease
in immunologically inexperienced mice. Surviving mice (or if endemic disease),
exhibit suppurative polyarthritis, swelling and loss of digits or limbs.
DISEASE
IN MAN:
Acute febrile disease following bite from a rodent. Can see inflammation,
lymphadenopathy, and nonspecific signs. May exhibit rash on extremities,
often soles and palms. May see arthritis with S. moniliformis. Incubation
period variable: S. moniliformis: hours to 1 to 3 days S. minus: 1 to 6 weeks
Symptoms usually resolve spontaneously. Complications, if not treated promptly,
lead to pneumonia, hepatitis, enteritis, endocarditis with a 10% fatality
rate.
DIAGNOSIS:
Culture: S. moniliformis requires 10 to 20% horse or rabbit serum
and reduced oxygen tension. S. minus- won't grow in vitro. Must inoculate
culture specimens into lab animals and use dark field microscopy.
TREATMENT:
Treat with procaine penicillin G or tetracycline HCl. Give supportive
and symptomatic measures as indicated.
PREVENTION/CONTROL:
Bacteriologic monitoring Proper treatment of rodent bites
PASTEURELLOSIS
Disease Overview: Institutional Animal Care
and Use Committee, University of California, Santa Barbara.
(Shipping or transport fever, hemorrhagic septicemia)
AGENT:
Pasteurella multocida, small, nonmotile, polymorphic, gram-positive
bacilli.
RESERVOIR
AND INCIDENCE
Inhabits the oral cavity and upper respiratory tract of many animals
(Rabbits, rodents, dogs, cats, mice, birds, swine). Dogs and cats are frequently
healthy carriers.
TRANSMISSION:
All animals and birds may be colonized by pasteurellas, and human
infection occurs by wound infection from bites or scratches. Animal-to-animal
transmission may occur by ingestion and inhalation. 1986 case report of
meningitis in a woman who kissed her dog (cultured positive for organism)
and also had dental caries which was considered to be the route of infection.
DISEASE
IN ANIMALS:
can cause acute pneumonia or septicemic disease in many species.
May cause chronic infection of upper respiratory and middle ear especially
in the rabbit.
DISEASE
IN MAN:
Local inflammation occurs around the bite or scratch, possibly
leading to abscess formation with systemic symptoms.
TREATMENT:
Penicillin, tetracycline, or cephalosporin.
PREVENTION/CONTROL:
Proper treatment of bite Protective clothing (mask,gloves) Euthanize
aggressive dogs and cats. Vaccinate cattle and sheep.
CLOSTRIDIAL INFECTIONS
Disease Overview: Institutional Animal Care
and Use Committee, University of California, Santa Barbara.
(Clostridial myositis: black leg, malignant edema, gas gangrene.
Enterotoxemia: pulpy kidney, struck, lamb dysentery, braxy. Tetanus: lockjaw).
AGENT:
Clostridium tetani (horses)--tetanus Clostridium perfringens (cattle,
sheep)--gas gangrene Clostridium septicum (cattle) malignant edema.
RESERVOIR
AND INCIDENCE
Clostridia are normal intestinal flora and also survive by spores
in the soil.
TRANSMISSION:
Infection may be by contamination of deep, penetrating wounds to
cause tetanus, by ingestion of preformed toxin or spores which vegetate in
the digestive tract to cause enterotoxemia, or by ingestion of spores which
are carried by the blood to muscles where they remain dormant until activated
by trauma to produce necrotizing myositis. C. perfringens food poisoning
is due to spore contamination of foods which survive heating to vegetate
in unrefrigerated conditions. Neonatal tetanus in humans is frequently caused
by contamination of the umbilicus.
DISEASE
IN ANIMALS:
Tetanus: as in humans. In myositis (black leg) cases a limb is
still and painful with crepitus on palpation. Signs of toxemia. Rapidly fatal.
C. chauvoei, novyi, and septicum toxins produce massive muscle necrosis, often
with edema and SC gas formation. C. perfringens causes a variety of profound
toxemias with cloudy swelling of parenchymatous organs and excess fluids,
often bloodstained in serous cavities.
DISEASE
IN MAN:
Tetanus: painful toxic contractions of muscles and trismus. The
case fatality rate for tetanus is 30-90% even when treated. Gas gangrene:
fever, toxemia, painful edema spreading from the edges of wounds, interstitial
emphysema, neck stiffness. Food poisoning: vomiting and diarrhea of a few
days' duration.
TREATMENT:
Myositis: penicillin, adequate surgical debridement and exposure
of infected areas. Tetanus: immune globulin, penicillin, mechanical ventilation.
Spasms are controlled with chlorpromazine or diazepam combined with a sedative.
PREVENTION/CONTROL:
Immunization with toxoids (good for 10 years), proper treatment
of wounds. Good food hygiene is essential. In animals, prevent wound contamination
during lambing, shearing, castration and docking.
CAPNOCYTOPHAGA
Disease Overview: Institutional Animal Care
and Use Committee, University of California, Santa Barbara.
AGENT:
Capnocytophaga canimorsus (formerly Dysgonic fermenter-2), a recently
described aerobic, gram negative bacillus with unusual fermentation pattern.
RESERVOIR
AND INCIDENCE
Found as part of oral flora of normal dogs and cats. C. canimorsus
has been isolated from the mouths of 24% and 17% of normal dogs and cats respectively.
Serious infections in man are most commonly reported in splenectomized or
immunocompromised people, alcoholics, or persons who have chronic respiratory
disease. More than 40 cases reported, many fatal, since first reported in
1976.
TRANSMISSION:
Contact, bite or scratch from dog or cat
DISEASE
IN MAN:
Can lead to cellulitis and overwhelming bacteremia, meningitis,
endocarditis, septic arthritis, and DIC. The organism appears to have an affinity
for the eye, causing angular blepharitis and severe keratitis. Accidental
corneal inoculation occurred during a tooth extraction in a Poodle causing
severe refractory keratitis in a veterinarian. The predisposition of the cornea
to infection may be due to its avascularity and to the low concentrations
of immunoglobulins and complement components in the tissue. Most serious disease
and fatalities have occurred in splenectomized people. Case fatality rates
of 4-27% have been reported.
DIAGNOSIS:
History, clinical signs, and culture. ORGANISM IS SLOW GROWING.
May require 8 days of incubation. Micro exam of blood smear or buffy coat
with gram stain to detect organisms.
PREVENTION/CONTROL:
Awareness, especially of high risk individuals Treatment of bite
wounds, Penicillin G. (Treatment of high risk people even without sign of
infection recommended).
PSITTACOSIS
Centers for Disease Control and Prevention: Division of Bacterial
and Mycotic Diseases
Psittacosis
Disease Overview: Institutional Animal Care
and Use Committee, University of California, Santa Barbara.
(Ornithosis, Parrot Fever, Chlamydiosis)
AGENT:
Obligate,intracellular organism with a unique development cycle
and worldwide distribution Genus Chlamydia has only four species, many strains
1. Chlamydia trachomatis- humans, mice (Zoonotic potential not known) 2. Chlamydia
psittaci- BIRDS, Mice, g. pig, rabbits, cats, frogs, ruminants 3. Chlamydia
pneumoniae- humans 4. Chlamydia pecorum- ruminants.
RESERVOIR
AND INCIDENCE
The mammalian strains appear to be a zoonotic problem only rarely.
2 cases of human conjunctivitis reported from close association with cats
with chlamydial pneumonitis and conjunctivitis. Birds are the main reservoir
of human infection, however, 25% of human cases have no history of avian contact.
Ovine strains may infect pregnant women.
TRANSMISSION:
Inhalation; dry feces produce highly infective aerosols Direct
contact with feces or respiratory secretions May survive in dust for several
months.
DISEASE
IN ANIMALS:
There are many strains of C. psittaci which produce a diverse disease
spectrum in animals, e.g., conjunctivitis, air sacculitis, pericarditis,
hepatitis, meningoencephalitis, enteritis, urethritis, arthritis, and endometritis
with abortion. G.I. infection results in enteric shedding of the organism.
Latency - Well recognized feature of Chlamydia infection, i.e., the organism
can cause inapparent infection or fulminant infection in the same host.
In clinically healthy birds, stress can precipitate clinical signs and shedding
of the organism.
DISEASE
IN MAN:
Asymptomatic or clinical disease after 1-2 week incubation period.
Fever, chills, myalgia, anorexia, headache, nonproductive cough. Pneumonitis
or atypical pneumonia may be present. May see a toxic or septic form with
hepatosplenomegaly, hepatitis, meningoencephalitis and cardiac involvement
with endocarditis. Ovine chlamydial infection in pregnant women is life-threatening,
causing late abortion and neonatal death and disseminated intravascular
coagulation in the mother.
DIAGNOSIS:
Fecal culture (rarely successful) serology (CF, IFA) [Note: African
Grey Parrot, cockatiel, and budgie may remain serologically negative despite
active infection.] ELISA-based tests for antigen in feces has proven reliable.
TREATMENT:
Tetracycline or Erythromycin.
PREVENTION/CONTROL:
Treatment with tetracycline Introduce birds into colony from psittacosis-free
flocks or use chlortetracycline chemoprophylaxis. Protective clothing (masks,
gowns, gloves). Wild caught birds should be placed on chlortetracycline
during quarantine. In sheep, keep flocks closed or vaccinate annually. Isolate
aborting ewes until discharges cease.
BLASTOMYCOSIS
Centers for Disease Control and Prevention: Division of Bacterial
and Mycotic Diseases
Blastomycosis
Disease Overview: Institutional Animal Care
and Use Committee, University of California, Santa Barbara.
SYNONYMS:
North American blastomycosis, Chicago disease, Gilchrist's disease.
ETIOLOGY:
Blastomyces dermatitidis, a dimorphic fungus existing in mycelial
form in cultures and as a budding yeast in the tissues of infected mammals.
GEOGRAPHIC
DISTRIBUTION:
The disease has been observed in the United States, eastern Canada,
Zaire, Tanzania, South Africa, and Tunisia. Autochthonous cases may have occurred
in some Latin American countries.
THE DISEASE
IN MAN:
The incubation period is not well known; it possibly extends to
several weeks or months. Blastomycosis is a chronic disease that principally
affects the lungs. The respiratory symptomatology initially resembles influenzas
purulent or bloody expectoration, weight loss, and cachexia, in addition to
fever and cough, may develop later. If the infection remains localized, it
can become asymptomatic. When it disseminates, it can cause subcutaneous
abscesses as well as localized infections in several organs. Death frequently
results in cases of untreated disseminated infection. The cutaneous form
is commonly secondary to the pulmo-nary and is characterized by an irregular-shaped,
scabby ulcer that has raised borders and contains minute abscesses. Lesions
develop on exposed parts of the body.
THE DISEASE
IN ANIMALS:
The highest incidence is observed in dogs around 2 years of age.
The symptoms consist of weight loss, chronic cough, dyspnea, cutaneous abscesses,
fever, anorexia, and sometimes blindness. The lesions localize in the lungs,
lymph nodes, eyes, skin, and joints and bones. Of 47 clinical cases recently
described, 72% occurred in large males. There were lesions of the respiratory
tract in 85% of the cases.
SOURCE
OF INFECTION AND MODE OF TRANSMISSION:
The reservoir is environmental, probably the soil, but the ecologic
biotope has not been determined. Transmission to man and to animals is effected
by aerosols; the fungal conidia are the infecting element. Persons at highest
risk are those having the most contact with the soil. Dogs most frequently
infected are sporting and hunting breeds.
ROLE OF
ANIMALS IN THE EPIDEMIOLOGY OF THE DISEASE:
None. It is a disease common to man and animals. Cases of transmission
from individual to individual (man or animal) are not known.
DIAGNOSIS:
Diagnosis is based on direct microscopic examination of sputum
and material from lesions, on isolation of the agent in culture media, and
on examination of histologic preparations. B. dermatitidis grows well in Sabouraud's
culture medium or other adequate median it is most distinctive in its sprouting
yeast form, and therefore the inoculated medium should be incubated at 37oC,
since at ambient temperature the mycelial form of the fungus is obtained.
B. dermatitidis in its yeast form (in tissues or cultures at 37oC) is characterized
by a single bud attached to the parent cell by a wide base, from which it
detaches when it has reached a size similar to the parent cell. In contrast,
Paracoccidioides brasiliensis, the agent of paracoccidioidomycosis ("South
American blastomycosis"), has multiple buds in the yeast phase. Serologic
tests in use are complement fixation and gel immunodiffusion; the latter
gives better results. It should be borne in mind that cross-reactions with
Histoplasma and Coccidioides may occur. At present, the intradermal test
is considered to have no diagnostic value.
TREATMENT:
Humans. Itraconazole, 100-200 mg/d orally, is now the therapy of
choice for nonmeningeal disease, with a response rate of over 70%. Amphotericin
B is given for treatment failures or cases with central nervous system involvement.
Follow-up for relapse should be regularly made for several years so that
therapy may be resumed or another drug instituted. Animals. Rare primary
cutaneous disease may persist for months; these lesions should be removed
surgically since blastomycosis responds poorly to therapy. Amphotericin
B is considered the drug of choice, but treatment is of little avail once
the disease is disseminated. The combination of amphotericin B and ketoconazole
has been suggested to reduce the rate of relapse.
CONTROL:
As long as the ecologic biotope remains poorly defined, practical
prevention methods cannot be established.
CAT SCRATCH DISEASE
Centers for Disease Control and Prevention: National Center for
Infectious Diseases
Cat Scratch
Disease (Bartonella henselae Infection)
Disease Overview: Institutional Animal Care
and Use Committee, University of California, Santa Barbara.
(Cat Scratch Fever, Benign Lymphoreticulosis, Benign nonbacterial
Lymphadenitis, Bacillary Angiomatosis, Bacillary Peliosis Hepatis)
AGENT:
Controversial, it is not currently possible to definitively name
the causative agent responsible for CSD. Felt to be either Afipia felis, a
gram-negative rod or Rochalimaea henselae and Rochalimaea quintana. Both are
members of class Proteobacteria and both are intracellular parasitic bacteria.
RESERVOIR
AND INCIDENCE
Associated with domestic cats throughout the USA, and worldwide.
Over 6000 cases annually. Seen more often in men than in women . Have seen
clusters of infection within families within a 2 to 3 week period, suggesting
that shedding by cats may occur periodically. Other sources of infection have
included scratches from other species including dogs, squirrels, and goats
and from wounds induced by crab claws, barbed wire, and plant material.
TRANSMISSION:
90% of patients have been exposed to a cat. 75% of these have been
bitten, scratched, or licked. Most affected individuals are <20 years of
age. 75-80% of the cases of CSD are diagnosed between September and February
with a peak incidence in December. 4 to 6% of the general population and 20%
of veterinarians have positive skin test reactions to CSD antigen.
DISEASE
IN ANIMALS:
Subclinical
DISEASE
IN MAN:
Different distinct syndromes exist:
Typical CSD
A primary lesion, most common on neck or extremities, will develop
in 50% of the cases and appear approximately 10 days after a bite or scratch.
A pustule persists for 1-2 weeks. 10-14 days after the lesion appears, lymphadenopathy
develops and usually regresses within 6 weeks. 30-50% of the enlarged nodes
become suppurative. Of the approximately 65% who develop systemic illness,
fever and malaise are the symptoms most often noted. The disease is usually
benign and most patients recover spontaneously without sequelae within 2-4
months. Many unrecognized cases probably occur. Disease appears to confer
lifelong immunity.
Atypical CSD
The atypical forms of CSD, which constitute 11% of all cases, are
extremely varied. The most common, representing 6% of all cases, is Parinaud's
oculoglandular syndrome (POGS), or granulomatous conjunctivitis with preauricular
adenopathy. Other, atypical presentations include tonsillitis, encephalitis,
cerebral arteritis, transverse myelitis, radiculitis, granulomatous hepatitis
and/or splenitis, osteolysis, atypical pneumonia, hilar adenopathy, pleural
effusion, erythema nodosum, erythema annulare, maculopapular rash, thrombocytopenic
purpura, and breast tumor. Bacillary Angiomatosis Dermal BA presents in
several ways. The commonest form is an enlarging red papule with some resemblance
to a cranberry, often with a collarette of scale and sometimes with a suggestion
of surrounding erythema. This type of lesion may be mistaken for pyogenic
granuloma, unless fairly deep biopsy specimens are examined. These lesions
begin as small papules and enlarge, occasionally becoming several centimeters
in diameter and rarely ulcerating. They may be single or quite numerous.
Another form of dermal BA is a deeper, subcutaneous nodule that appears flesh-colored
and may be either fixed to subcutaneous tissues or freely mobile. Rarely BA
may present as a dermal plaque. BA has been reported to occur in every organ
system, including the brain, and is often difficult to differentiate from
mycobacterial and fungal infections or malignancy without the use of biopsy.
It is unclear if the personality changes, ranging from frank psychosis to
depression, that have been described in association with BA represent CNS
involvement or a neurotoxic product of this infection. Bacillary Peliosis
Hepatis BPH, a vasoproliferative condition involving the liver of HIV-infected
patients, is characterized by a proliferation of cystic blood-filled spaces
surrounded by fibromyxoid stroma in which one can see bacteria similar to
those seen in BA. Clinically these patients may or may not have visible bacillary
angiomas. Their symptoms usually include fever, weight loss, and abdominal
pain or fullness. Physical exam may reveal organomegaly. Laboratory studies
usually demonstrate elevation of alkaline phosphatase and ç-glutamyltransferase
levels out of proportion to those of aminotransferase and bilirubin.
DIAGNOSIS:
The sedimentation rate is elevated, the white blood cell count
normal, and the pus from the nodes is sterile. ID skin testing with antigen
prepared from the pus is positive. Excisional biopsy, usually performed to
exclude lymphoma, confirms the diagnosis.
TREATMENT:
For CSD: Rifampin, ciprofloxacin, gentamycin, and trimethoprim-sulfa.
Aspiration of suppurating nodes is recommended for relief of pain. Symptoms
resolve without treatment in 2-4 months. BA and BPH respond to erythromycin,
rifampin, or doxycycline. Therapy must be continue for 4-6 weeks to avoid
relapse.
PREVENTION/CONTROL:
Education. Wash hands after handling cat. Wash cuts and scratches
promptly and don't allow cat to lick open wound.
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